Cell labeling with magnetic iron oxide nanoparticles(IONPs)is increasingly a routine approach in the cellbased cancer treatment.However,cell labeling with magnetic IONPs and their leading effects on the biological pro...Cell labeling with magnetic iron oxide nanoparticles(IONPs)is increasingly a routine approach in the cellbased cancer treatment.However,cell labeling with magnetic IONPs and their leading effects on the biological properties of human lung carcinoma cells remain scarcely reported.Therefore,in the present study the magnetic c-Fe2O3nanoparticles(MNPs)were firstly synthesized and surface-modified with cationic poly-L-lysine(PLL)to construct the PLL-MNPs,which were then used to magnetically label human A549 lung cancer cells.Cell viability and proliferation were evaluated with propidium iodide/fluorescein diacetate double staining and standard 3-(4,5-dimethylthiazol-2-diphenyl-tetrazolium)bromide assay,and the cytoskeleton was immunocytochemically stained.The cell cycle of the PLL-MNPlabeled A549 lung cancer cells was analyzed using flow cytometry.Apoptotic cells were fluorescently analyzed with nuclear-specific staining after the PLL-MNP labeling.The results showed that the constructed PLL-MNPs efficiently magnetically labeled A549 lung cancer cells and that,at low concentrations,labeling did not affect cellular viability,proliferation capability,cell cycle,and apoptosis.Furthermore,the cytoskeleton in the treated cells was detected intact in comparison with the untreated counterparts.However,the results also showed that at high concentration(400 lg m L-1),the PLL-MNPs would slightly impair cell viability,proliferation,cell cycle,and apoptosis and disrupt the cytoskeleton in the treated A549 lung cancer cells.Therefore,the present results indicated that the PLL-MNPs at adequate concentrations can be efficiently used for labeling A549 lung cancer cells and could be considered as a feasible approach for magnetic targeted anti-cancer drug/gene delivery,targeted diagnosis,and therapy in lung cancer treatment.展开更多
BACKGROUND Lung cancer is one of the deadliest cancers in the world with the highest incidence and mortality rate among all cancers.Non-small cell lung cancer(NSCLC)accounts for approximately 80%of primary lung cancer...BACKGROUND Lung cancer is one of the deadliest cancers in the world with the highest incidence and mortality rate among all cancers.Non-small cell lung cancer(NSCLC)accounts for approximately 80%of primary lung cancer.However,efficacy and safety of the current regimens for NSCLC is unsatisfactory.Therefore,there has been an increasing urgency for development of potential therapeutic therapies for NSCLC.AIM To investigate the therapeutic outcomes and safety of continuous intravenous infusion of recombinant human endostatin(Rh-endostain)using an infusion pump in retreated advanced NSCLC.METHODS Patients with retreated advanced NSCLC who were admitted to Zhejiang Provincial People's Hospital from October 2017 to April 2019 were recruited.These patients received continuous intravenous infusion of Rh-endostain using an infusion pump.Objective response rate(ORR),clinical benefit rate(CBR),median progression-free survival(mPFS),and incidences of adverse events(AEs)were analyzed after treatment.RESULTS A total of 45 patients with retreated advanced NSCLC were included,and all of them were evaluated.In these patients,ORR was 22.2%,CBR was 84.4%,and mPFS was 5.3 mo.The following AEs were observed,decreased hemoglobin(34 cases,75.6%),nausea/vomiting(32 cases,71.1%),elevated transaminase(24 cases,53.3%),leukopenia(16 cases,35.6%),thrombocytopenia(14 cases,31.1%),and constipation(1 case,3.4%).None of the patients had leukopenia,nausea/vomiting,and constipation of grade III and above.CONCLUSION The patients showed improved adherence to 5-d continuous intravenous infusion of Rh-endostain using an infusion pump.Favorable efficacy and safety of this treatment regimen were achieved in retreated advanced NSCLC.展开更多
Backgroud and Objective Tumor metastasis is not only the malignant marker and characteristics of lung cancer, but also the main cause of failure to cure and lose their life of the
Human LAK cells were prepared by culturing normal human peripheral blood mononuclear cells (PBMC) with or without rIL-2 and assayed for T cell surface markers as well as anti-tumor activity against PC in vitro and in ...Human LAK cells were prepared by culturing normal human peripheral blood mononuclear cells (PBMC) with or without rIL-2 and assayed for T cell surface markers as well as anti-tumor activity against PC in vitro and in nude mice. Although the percentages of T3, T4, and T8 positive cells in rIL-2-activated cells did not differ significantly from those of control cells in vitro, the former showed stronger cytotoxicity than control cells to PG tumor cells in vitro. In vivo, LAK cells completely inhibited the growth of PG tumor in nude mice, whereas PBMC control cells were to be of no effect. The anti-tumor effect of human LAK cells in nude mice may offer a useful model to study the role of human LAK cells against human tumor in vivo.展开更多
Objective:To investigate the effects of recombinant human endostatin on therapeutic effect, angiogenesis, tumor cell proliferation and migration in patients with non-small cell lung cancer.Methods: A total of 100 pati...Objective:To investigate the effects of recombinant human endostatin on therapeutic effect, angiogenesis, tumor cell proliferation and migration in patients with non-small cell lung cancer.Methods: A total of 100 patients with non-small cell lung cancer treated in our hospital from September 2015 to March 2018 were selected as research subjects.They were randomly divided into observation group and control group, 50 cases in each group.The control group was treated with gemcitabine plus cisplatin, while the observation group was combined with Endostar treatment on the basis of the control group. Observed and compared the expression of the therapeutic effect[including cytokeratin 19 fragment (CYFRA21-1), carcinoembryonic antigen (CEA) and carbohydrate antigen (CA50)], angiogenesis[including vascular endothelial growth factor (VEGF) and hypoxia inducible factor (HIF-1 alpha)], tumor cell proliferation[including insulin-like growth factor (IGF-1) and insulin-like growth factor receptor -7 (IGFBP-7)] and migration[including high mobility group protein AT-hook2 (HMGA2) and high mobility group protein B1 (HMGB1)]in two groups.Results: The two groups showed significant changes in the therapeutic effect, angiogenesis, proliferation and migration of tumor cells. Before treatment, there was no significant difference in all levels between the two groups. After treatment, the levels of CYFRA21-1, CEA, CA50, VEGF, HIF-1a, IGF-1, HMGA2 and HMGB1 in the two groups were significantly lower than those before treatment, while the levels of IGFBP-7 were significantly higher than those before treatment. After treatment, the levels of CYFRA21-1, CEA, CA50, VEGF, HIF-1a, IGF-1, HMGA2 and HMGB1 in the observation group were significantly lower than those in the control group, while the levels of IGFBP-7 were significantly higher than those in the control group. Conclusions: Recombinant human endostatin can enhance the therapeutic effect of non-small cell lung cancer patients, reduce angiogenesis, inhibit tumor cell proliferation and migration.展开更多
Background and Objective Lung cancer is the most lethal malignangy that threatens human heath and lives nowadays in the world, and meanwhile is also the one with worst
Background and Objective It has been proven that copy number gain/or loss (copy number variation CNV) in uences gene expression and result in phenotypic variation by
Background and Objective Lung cancer has the fastest increasing rate of morbidity and mortality all over the world and appears to be one of the most dangerous malignant tumors
Background and Objective Lung cancer is the rst killer of human being in the whole world. Recently, although many treatment strategies have been developed, the anti-cancer effects
Backgroud and Objective Tumor metastasis is not only the malignant marker and characteristics of lung cancer, but also the key cause of failure to cure and lose their life of the patients
Background and Objective Invasion and metastasis is not only the malignant phenotypes of lung cancer but also the main cause of death. To study and elucidate the molecular mechanism
Objective To explore the inhibition mechanism and safety of pyrazolo[1,5-a]pyrazin-4(5H)-one derivatives against proliferation of human lung cancer A549 cells, H322 cells, and human umbilical vein endothelial cell(HUV...Objective To explore the inhibition mechanism and safety of pyrazolo[1,5-a]pyrazin-4(5H)-one derivatives against proliferation of human lung cancer A549 cells, H322 cells, and human umbilical vein endothelial cell(HUVEC). Methods Cells were treated with 40 μmol/L of the ppo3 a, ppo3 b, ppo3 i, and 0.1% DMSO(control) for 48 hours, respectively. Apoptosis was determined by Hoechst 33258 staining assay in H322 and A549 cells. Cell cycle distribution was determined by flow cytometry analysis in A549 cell. LC3-II, p53, and heat shock protein(HSP) 70 protein levels were detected by Western blotting in A549 cells treated with ppo3 b for 48 hours. The morphology and viability of HUVEC were observed by inverted microscope and sulforhodamine B(SRB) assay. Results Ppo3 a, ppo3 b, and ppo3 i significantly induced apoptosis in H322 and A549 cells. A strong G1-phase arrest was concomitant with the growth inhibitory effect on A549 cells. Ppo3 b effectively elevated the p53 protein level, but significantly reduced the HSP70 protein level. There were no significantly inhibitory effect on the morphology and viability of HUVEC when treated with ppo3 a, ppo3 b, and ppo3 i. Conclusions ppo3 a, ppo3 b, and ppo3 i could inhibit H322 proliferation through apoptosis and inhibit A549 through apoptosis and G1-phase arrest. The protein p53 and HSP70 might involve in the inhibition effects. These derivatives might be a clue to find effective and safe drug for lung cancers.展开更多
Objective: To study the value of serum NGAL and HE4 content change for diagnosing non-small cell lung cancer (NSCLC) and evaluating disease progression. Methods: Patients who were diagnosed with NSCLC and underwent su...Objective: To study the value of serum NGAL and HE4 content change for diagnosing non-small cell lung cancer (NSCLC) and evaluating disease progression. Methods: Patients who were diagnosed with NSCLC and underwent surgical resection in the First Affiliated Hospital of Chengdu Medical College between February 2015 and March 2017 were selected as the NSCLC group, and healthy volunteers who received physical examination over the same period were selected as control group. The NGAL and HE4 contents in serum of NSCLC group and control group as well as the expression of proliferation, apoptosis and invasion genes in NSCLC lesion of NSCLC group were detected. Results: Serum NGAL and HE4 levels of NSCLC group were significantly higher than those of control group, serum NGAL and HE4 levels of patients with TNM II and TNM III NSCLC were significantly higher than those of patients with TNM I NSCLC, and serum NGAL and HE4 levels of patients with TNM III NSCLC were significantly higher than those of patients with TNM II NSCLC;c-myc, Survivin, CatL, Vimentin, Slug and Snail mRNA expression in NSCLC lesion were significantly higher than those in adjacent lesion and positively correlated with serum NGAL and HE4 levels while PTEN, LATS1 and E-cadherin mRNA expression were significantly lower than those in adjacent lesion and negatively correlated with serum NGAL and HE4 levels. Conclusion: Abnormally elevated NGAL and HE4 in the serum of NSCLC patients can evaluate the proliferation and invasion of cancer cells to a certain extent.展开更多
Objective： To study the inhibition of Cantharidin against the proliferation of human lung cancer A549 cells and its mechanism. Methods： MTT assay was employed to determine the inhibition of Cantharidin against proli...Objective： To study the inhibition of Cantharidin against the proliferation of human lung cancer A549 cells and its mechanism. Methods： MTT assay was employed to determine the inhibition of Cantharidin against proliferation of A549 cells and flow Cytometry was applied to analyze A549 cell cycle and the effect of Cantharidin on cell cycle. Results： Cantharidin showed inhibition against the proliferation of A549 cells, and the inhibition was mediated by blocking A549 cell cycle at G2/M phase significantly. Conclusion： Cantharidin exhibits inhibition against the proliferation of human lung cancer A549 cells.展开更多
A cell line derived from human lung cancer(AOI) was employed in the present study.A panel of cytokines were quantified by ELISA technique following cellular exposure to X-irradiation.
Objective： To evaluate the cytotoxic effects of ampelopsin sodium（Amp-Na） and carboplatin（CBP） used alone or in combination on human non-small cell lung cancer（NSCLC） cells SPC-A1 in vitro and its related mecha...Objective： To evaluate the cytotoxic effects of ampelopsin sodium（Amp-Na） and carboplatin（CBP） used alone or in combination on human non-small cell lung cancer（NSCLC） cells SPC-A1 in vitro and its related mechanism. Methods： Cytotoxic effects were assessed by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide（MTT） assays. The synergistic effects of the drugs were calculated with coefficient of drug interaction（CDI）. Cell cycle was determined by flow cytometry（FCM）. The levels of p53, p21, cyclin E, cyclin D1, and phosphorylated cyclin-dependent kinase-2（p-CDK2） were evaluated by Western blot. Results： Amp-Na（6.25–200 μg/m L） and CBP（3.13–100 μg/m L） alone exhibited prominent cytotoxic activity in a concentration-dependent manner on SPC-A1 cells with 50% inhibitive concentration values of 57.07±14.46 and 34.97±6.30 μg/m L, respectively. Drug combinations were associated with significantly higher cytotoxic effects than each drug alone（P〈0.05 or 0.01）. The CDI analysis confirmed the synergy of Amp-Na and CBP on inhibiting cancer cell viability across a wide concentration range（CDI 〈1）. FCM and Western blot showed that synergistic cytotoxic effects of Amp-Na and CBP were related to G1 arrested which mainly mediated by p21 through the inhibition of CDK2 activity independent of the p53 tumor suppressor pathway. Conclusions： AmpNa exhibits anticancer activities and enhances the antitumor activities of CBP through up-regulation of p21 and inhibition of CDK2 activity in human NSCLC cells SPC-A1. These results suggest that Amp-Na may be applied to enhance the anticancer action of CBP.展开更多
Recently,we found that high concentration of taxol(70μM)induced cell death with cytoplasm vacuolization,the typical characteristic of both paraptosis and oncosis,in human lung carcinoma(ASTC-a-1)cells.This report was...Recently,we found that high concentration of taxol(70μM)induced cell death with cytoplasm vacuolization,the typical characteristic of both paraptosis and oncosis,in human lung carcinoma(ASTC-a-1)cells.This report was designed to further deternine the form of taxo-induced cell death with cytoplasm vacuolization.It is generally coneidered that the cytoplasm vacuolization in oncosis due to the sweling of endoplasmic reticulum(ER),mitochondria,lysosomes and muclei occurs after the loss of mitochondrial mermbrane potential(△ψm).However,flow cytometry(FCM)analysis showed that taxol induced cy toplsm vacuolization preceded the loss of(△ψm).Moreover,taxol treatment did not induce the collapse of microtubule,the ty pical characteristic of oncosis.These data demonstrated that taxol-induced cell death with cytoplasm vacuolization is not onoosis.FCM analysis by Annexin V-FTTC/PI apoptosis detection kit further demoustrated that taxol-induced cell death with cytoplasm vacuolization is not apoptosis.In conclusion,in combination with our recent in ritro and in vito data,this report further demonstrates that high concentration of taxol induces cell death with cytoplasm vacuolization in paraptosis like but not oncosis fashion.展开更多
We examined the possibility that the anti-estrogens, tamoxifen (TX) and toremifen (TO) interacted?with the immune system. Indeed, both TX and TO stimulated cells mediated cytotoxicity reactions by various killer cells...We examined the possibility that the anti-estrogens, tamoxifen (TX) and toremifen (TO) interacted?with the immune system. Indeed, both TX and TO stimulated cells mediated cytotoxicity reactions by various killer cells: killer T (TK), natural killer (NK), lymphokine activated killer (LAK) cells. Both TX and TO inhibited the growth of tumors that express estrogen receptors. Thus these antiestrogens inhibited tumor growth and stimulated killer cells for cytotoxicty on such tumors. Therefore these agents were presumed to stimulate tumor immunity. We tested the P815 mouse mastcytoma with TK, LK, and TX or TO. A therapeutic effect was observed in both experiments. The SL2-5 murine lymphoma was tested with NK and TX cells or TO cells and successful immunotherapy was observed.?We digested human breast carcinomas and lung tumors with collagenase. The killer cells were separated from tumor cells on Ficoll gradients. TX and TO enhanced the cytotoxic effect of autologous killer cells on the corresponding tumor cells. This experiment indicates that the results obtained in animals are also valid for human malignant disease.展开更多
基金supported by the National Natural Science Foundation of China(No.314 008 55)the Technological Innovation Incubator Program from Henan University of Technology(No.201 518)the Introduced Postdoctoral Talents of Henan University of Technology(No.150 199)
文摘Cell labeling with magnetic iron oxide nanoparticles(IONPs)is increasingly a routine approach in the cellbased cancer treatment.However,cell labeling with magnetic IONPs and their leading effects on the biological properties of human lung carcinoma cells remain scarcely reported.Therefore,in the present study the magnetic c-Fe2O3nanoparticles(MNPs)were firstly synthesized and surface-modified with cationic poly-L-lysine(PLL)to construct the PLL-MNPs,which were then used to magnetically label human A549 lung cancer cells.Cell viability and proliferation were evaluated with propidium iodide/fluorescein diacetate double staining and standard 3-(4,5-dimethylthiazol-2-diphenyl-tetrazolium)bromide assay,and the cytoskeleton was immunocytochemically stained.The cell cycle of the PLL-MNPlabeled A549 lung cancer cells was analyzed using flow cytometry.Apoptotic cells were fluorescently analyzed with nuclear-specific staining after the PLL-MNP labeling.The results showed that the constructed PLL-MNPs efficiently magnetically labeled A549 lung cancer cells and that,at low concentrations,labeling did not affect cellular viability,proliferation capability,cell cycle,and apoptosis.Furthermore,the cytoskeleton in the treated cells was detected intact in comparison with the untreated counterparts.However,the results also showed that at high concentration(400 lg m L-1),the PLL-MNPs would slightly impair cell viability,proliferation,cell cycle,and apoptosis and disrupt the cytoskeleton in the treated A549 lung cancer cells.Therefore,the present results indicated that the PLL-MNPs at adequate concentrations can be efficiently used for labeling A549 lung cancer cells and could be considered as a feasible approach for magnetic targeted anti-cancer drug/gene delivery,targeted diagnosis,and therapy in lung cancer treatment.
文摘BACKGROUND Lung cancer is one of the deadliest cancers in the world with the highest incidence and mortality rate among all cancers.Non-small cell lung cancer(NSCLC)accounts for approximately 80%of primary lung cancer.However,efficacy and safety of the current regimens for NSCLC is unsatisfactory.Therefore,there has been an increasing urgency for development of potential therapeutic therapies for NSCLC.AIM To investigate the therapeutic outcomes and safety of continuous intravenous infusion of recombinant human endostatin(Rh-endostain)using an infusion pump in retreated advanced NSCLC.METHODS Patients with retreated advanced NSCLC who were admitted to Zhejiang Provincial People's Hospital from October 2017 to April 2019 were recruited.These patients received continuous intravenous infusion of Rh-endostain using an infusion pump.Objective response rate(ORR),clinical benefit rate(CBR),median progression-free survival(mPFS),and incidences of adverse events(AEs)were analyzed after treatment.RESULTS A total of 45 patients with retreated advanced NSCLC were included,and all of them were evaluated.In these patients,ORR was 22.2%,CBR was 84.4%,and mPFS was 5.3 mo.The following AEs were observed,decreased hemoglobin(34 cases,75.6%),nausea/vomiting(32 cases,71.1%),elevated transaminase(24 cases,53.3%),leukopenia(16 cases,35.6%),thrombocytopenia(14 cases,31.1%),and constipation(1 case,3.4%).None of the patients had leukopenia,nausea/vomiting,and constipation of grade III and above.CONCLUSION The patients showed improved adherence to 5-d continuous intravenous infusion of Rh-endostain using an infusion pump.Favorable efficacy and safety of this treatment regimen were achieved in retreated advanced NSCLC.
基金supported by grants from National Natural Sciences Foundation of China (to Qinghua ZHOU, No.3007033 )
文摘Backgroud and Objective Tumor metastasis is not only the malignant marker and characteristics of lung cancer, but also the main cause of failure to cure and lose their life of the
文摘Human LAK cells were prepared by culturing normal human peripheral blood mononuclear cells (PBMC) with or without rIL-2 and assayed for T cell surface markers as well as anti-tumor activity against PC in vitro and in nude mice. Although the percentages of T3, T4, and T8 positive cells in rIL-2-activated cells did not differ significantly from those of control cells in vitro, the former showed stronger cytotoxicity than control cells to PG tumor cells in vitro. In vivo, LAK cells completely inhibited the growth of PG tumor in nude mice, whereas PBMC control cells were to be of no effect. The anti-tumor effect of human LAK cells in nude mice may offer a useful model to study the role of human LAK cells against human tumor in vivo.
文摘Objective:To investigate the effects of recombinant human endostatin on therapeutic effect, angiogenesis, tumor cell proliferation and migration in patients with non-small cell lung cancer.Methods: A total of 100 patients with non-small cell lung cancer treated in our hospital from September 2015 to March 2018 were selected as research subjects.They were randomly divided into observation group and control group, 50 cases in each group.The control group was treated with gemcitabine plus cisplatin, while the observation group was combined with Endostar treatment on the basis of the control group. Observed and compared the expression of the therapeutic effect[including cytokeratin 19 fragment (CYFRA21-1), carcinoembryonic antigen (CEA) and carbohydrate antigen (CA50)], angiogenesis[including vascular endothelial growth factor (VEGF) and hypoxia inducible factor (HIF-1 alpha)], tumor cell proliferation[including insulin-like growth factor (IGF-1) and insulin-like growth factor receptor -7 (IGFBP-7)] and migration[including high mobility group protein AT-hook2 (HMGA2) and high mobility group protein B1 (HMGB1)]in two groups.Results: The two groups showed significant changes in the therapeutic effect, angiogenesis, proliferation and migration of tumor cells. Before treatment, there was no significant difference in all levels between the two groups. After treatment, the levels of CYFRA21-1, CEA, CA50, VEGF, HIF-1a, IGF-1, HMGA2 and HMGB1 in the two groups were significantly lower than those before treatment, while the levels of IGFBP-7 were significantly higher than those before treatment. After treatment, the levels of CYFRA21-1, CEA, CA50, VEGF, HIF-1a, IGF-1, HMGA2 and HMGB1 in the observation group were significantly lower than those in the control group, while the levels of IGFBP-7 were significantly higher than those in the control group. Conclusions: Recombinant human endostatin can enhance the therapeutic effect of non-small cell lung cancer patients, reduce angiogenesis, inhibit tumor cell proliferation and migration.
基金supported by a grant from the key project of the National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30430300)National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30670922)INTERNATION Scienc and Techniquie COOPRATION PROGRAM OF CHINA (ISCP) (to Qinghua ZHOU)(No.2006DFB32330)
文摘Background and Objective Lung cancer is the most lethal malignangy that threatens human heath and lives nowadays in the world, and meanwhile is also the one with worst
基金supported by a grant from the key project of the National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30430300)National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30670922)INTERNATION Scienc and Techniquie COOPRATION PROGRAM OF CHINA (ISCP) (to Qinghua ZHOU)(No.2006DFB32330)
文摘Background and Objective It has been proven that copy number gain/or loss (copy number variation CNV) in uences gene expression and result in phenotypic variation by
基金supported by a grant from the key project of the National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30430300)National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30670922)INTERNATION Scienc and Techniquie COOPRATION PROGRAM OF CHINA (ISCP) (to Qinghua ZHOU)(No.2006DFB32330)
文摘Background and Objective Lung cancer has the fastest increasing rate of morbidity and mortality all over the world and appears to be one of the most dangerous malignant tumors
基金supported by a grant from the key project of the National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30430300)National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30670922)INTERNATION Scienc and Techniquie COOPRATION PROGRAM OF CHINA (ISCP) (to Qinghua ZHOU)(No.2006DFB32330)
文摘Background and Objective Lung cancer is the rst killer of human being in the whole world. Recently, although many treatment strategies have been developed, the anti-cancer effects
基金supported by grants from the Key Project of National Natural Science Foundation of China (to Qinghua ZHOU) (No.30430300)National Natural Science Foundation of China (to Qinghua ZHOU) (No.30070333)
文摘Backgroud and Objective Tumor metastasis is not only the malignant marker and characteristics of lung cancer, but also the key cause of failure to cure and lose their life of the patients
基金supported by a grant from the key project of the National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30430300)National Natural Science Foundation of China (to Qinghua ZHOU)(No. 30670922)INTERNATION Scienc and Techniquie COOPRATION PROGRAM OF CHINA (ISCP) (to Qinghua ZHOU)(No.2006DFB32330)
文摘Background and Objective Invasion and metastasis is not only the malignant phenotypes of lung cancer but also the main cause of death. To study and elucidate the molecular mechanism
基金Supported by the Doctoral Research Fund of Hubei University of Art and Science(2013B009)the Post-doctoral Research Fund of Shandong University(111935)
文摘Objective To explore the inhibition mechanism and safety of pyrazolo[1,5-a]pyrazin-4(5H)-one derivatives against proliferation of human lung cancer A549 cells, H322 cells, and human umbilical vein endothelial cell(HUVEC). Methods Cells were treated with 40 μmol/L of the ppo3 a, ppo3 b, ppo3 i, and 0.1% DMSO(control) for 48 hours, respectively. Apoptosis was determined by Hoechst 33258 staining assay in H322 and A549 cells. Cell cycle distribution was determined by flow cytometry analysis in A549 cell. LC3-II, p53, and heat shock protein(HSP) 70 protein levels were detected by Western blotting in A549 cells treated with ppo3 b for 48 hours. The morphology and viability of HUVEC were observed by inverted microscope and sulforhodamine B(SRB) assay. Results Ppo3 a, ppo3 b, and ppo3 i significantly induced apoptosis in H322 and A549 cells. A strong G1-phase arrest was concomitant with the growth inhibitory effect on A549 cells. Ppo3 b effectively elevated the p53 protein level, but significantly reduced the HSP70 protein level. There were no significantly inhibitory effect on the morphology and viability of HUVEC when treated with ppo3 a, ppo3 b, and ppo3 i. Conclusions ppo3 a, ppo3 b, and ppo3 i could inhibit H322 proliferation through apoptosis and inhibit A549 through apoptosis and G1-phase arrest. The protein p53 and HSP70 might involve in the inhibition effects. These derivatives might be a clue to find effective and safe drug for lung cancers.
基金Youth Project of Natural Science Foundation of China(:81001345)Project of Science&Technology Department of Sichuan Province(:2014JY0039).
文摘Objective: To study the value of serum NGAL and HE4 content change for diagnosing non-small cell lung cancer (NSCLC) and evaluating disease progression. Methods: Patients who were diagnosed with NSCLC and underwent surgical resection in the First Affiliated Hospital of Chengdu Medical College between February 2015 and March 2017 were selected as the NSCLC group, and healthy volunteers who received physical examination over the same period were selected as control group. The NGAL and HE4 contents in serum of NSCLC group and control group as well as the expression of proliferation, apoptosis and invasion genes in NSCLC lesion of NSCLC group were detected. Results: Serum NGAL and HE4 levels of NSCLC group were significantly higher than those of control group, serum NGAL and HE4 levels of patients with TNM II and TNM III NSCLC were significantly higher than those of patients with TNM I NSCLC, and serum NGAL and HE4 levels of patients with TNM III NSCLC were significantly higher than those of patients with TNM II NSCLC;c-myc, Survivin, CatL, Vimentin, Slug and Snail mRNA expression in NSCLC lesion were significantly higher than those in adjacent lesion and positively correlated with serum NGAL and HE4 levels while PTEN, LATS1 and E-cadherin mRNA expression were significantly lower than those in adjacent lesion and negatively correlated with serum NGAL and HE4 levels. Conclusion: Abnormally elevated NGAL and HE4 in the serum of NSCLC patients can evaluate the proliferation and invasion of cancer cells to a certain extent.
文摘Objective： To study the inhibition of Cantharidin against the proliferation of human lung cancer A549 cells and its mechanism. Methods： MTT assay was employed to determine the inhibition of Cantharidin against proliferation of A549 cells and flow Cytometry was applied to analyze A549 cell cycle and the effect of Cantharidin on cell cycle. Results： Cantharidin showed inhibition against the proliferation of A549 cells, and the inhibition was mediated by blocking A549 cell cycle at G2/M phase significantly. Conclusion： Cantharidin exhibits inhibition against the proliferation of human lung cancer A549 cells.
文摘A cell line derived from human lung cancer(AOI) was employed in the present study.A panel of cytokines were quantified by ELISA technique following cellular exposure to X-irradiation.
基金Supported by the Natural Science Foundation of Gansu Province,China(No.0710RJZA044)
文摘Objective： To evaluate the cytotoxic effects of ampelopsin sodium（Amp-Na） and carboplatin（CBP） used alone or in combination on human non-small cell lung cancer（NSCLC） cells SPC-A1 in vitro and its related mechanism. Methods： Cytotoxic effects were assessed by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide（MTT） assays. The synergistic effects of the drugs were calculated with coefficient of drug interaction（CDI）. Cell cycle was determined by flow cytometry（FCM）. The levels of p53, p21, cyclin E, cyclin D1, and phosphorylated cyclin-dependent kinase-2（p-CDK2） were evaluated by Western blot. Results： Amp-Na（6.25–200 μg/m L） and CBP（3.13–100 μg/m L） alone exhibited prominent cytotoxic activity in a concentration-dependent manner on SPC-A1 cells with 50% inhibitive concentration values of 57.07±14.46 and 34.97±6.30 μg/m L, respectively. Drug combinations were associated with significantly higher cytotoxic effects than each drug alone（P〈0.05 or 0.01）. The CDI analysis confirmed the synergy of Amp-Na and CBP on inhibiting cancer cell viability across a wide concentration range（CDI 〈1）. FCM and Western blot showed that synergistic cytotoxic effects of Amp-Na and CBP were related to G1 arrested which mainly mediated by p21 through the inhibition of CDK2 activity independent of the p53 tumor suppressor pathway. Conclusions： AmpNa exhibits anticancer activities and enhances the antitumor activities of CBP through up-regulation of p21 and inhibition of CDK2 activity in human NSCLC cells SPC-A1. These results suggest that Amp-Na may be applied to enhance the anticancer action of CBP.
基金supported by National Natural Sci-ence Foundation of China(31071218 and 81071491)Key Project of the Department of Education and Finance of Guangdong Province(cxzd115).
文摘Recently,we found that high concentration of taxol(70μM)induced cell death with cytoplasm vacuolization,the typical characteristic of both paraptosis and oncosis,in human lung carcinoma(ASTC-a-1)cells.This report was designed to further deternine the form of taxo-induced cell death with cytoplasm vacuolization.It is generally coneidered that the cytoplasm vacuolization in oncosis due to the sweling of endoplasmic reticulum(ER),mitochondria,lysosomes and muclei occurs after the loss of mitochondrial mermbrane potential(△ψm).However,flow cytometry(FCM)analysis showed that taxol induced cy toplsm vacuolization preceded the loss of(△ψm).Moreover,taxol treatment did not induce the collapse of microtubule,the ty pical characteristic of oncosis.These data demonstrated that taxol-induced cell death with cytoplasm vacuolization is not onoosis.FCM analysis by Annexin V-FTTC/PI apoptosis detection kit further demoustrated that taxol-induced cell death with cytoplasm vacuolization is not apoptosis.In conclusion,in combination with our recent in ritro and in vito data,this report further demonstrates that high concentration of taxol induces cell death with cytoplasm vacuolization in paraptosis like but not oncosis fashion.
文摘We examined the possibility that the anti-estrogens, tamoxifen (TX) and toremifen (TO) interacted?with the immune system. Indeed, both TX and TO stimulated cells mediated cytotoxicity reactions by various killer cells: killer T (TK), natural killer (NK), lymphokine activated killer (LAK) cells. Both TX and TO inhibited the growth of tumors that express estrogen receptors. Thus these antiestrogens inhibited tumor growth and stimulated killer cells for cytotoxicty on such tumors. Therefore these agents were presumed to stimulate tumor immunity. We tested the P815 mouse mastcytoma with TK, LK, and TX or TO. A therapeutic effect was observed in both experiments. The SL2-5 murine lymphoma was tested with NK and TX cells or TO cells and successful immunotherapy was observed.?We digested human breast carcinomas and lung tumors with collagenase. The killer cells were separated from tumor cells on Ficoll gradients. TX and TO enhanced the cytotoxic effect of autologous killer cells on the corresponding tumor cells. This experiment indicates that the results obtained in animals are also valid for human malignant disease.
