BACKGROUND Gastric cancer is one of the most common malignant tumors of the digestive system worldwide,posing a serious danger to human health.Cyclooxygenase(COX)-2 plays an important role in the carcinogenesis and pr...BACKGROUND Gastric cancer is one of the most common malignant tumors of the digestive system worldwide,posing a serious danger to human health.Cyclooxygenase(COX)-2 plays an important role in the carcinogenesis and progression of gastric cancer.Acetyl-11-keto-β-boswellic acid(AKBA)is a promising drug for cancer therapy,but its effects and mechanism of action on human gastric cancer remain unclear.AIM To evaluate whether the phosphatase and tensin homolog(PTEN)/Akt/COX-2 signaling pathway is involved in the anti-tumor effect of AKBA in gastric cancer.METHODS Human poorly differentiated BGC823 and moderately differentiated SGC7901 gastric cancer cells were routinely cultured in Roswell Park Memorial Institute 1640 medium supplemented with 10%fetal bovine serum and 1%penicillin/streptomycin.Gastric cancer cell proliferation was determined by methyl thiazolyl tetrazolium colorimetric assay.Apoptosis was measured by flow cytometry.Cell migration was assessed using the wound-healing assay.Expression of Bcl-2,Bax,proliferating cell nuclear antigen,PTEN,p-Akt,and COX-2 were detected by Western blot analysis.A xenograft nude mouse model of human gastric cancer was established to evaluate the anti-cancer effect of AKBA RESULTS AKBA significantly inhibited the proliferation of gastric cancer cells in a dose-and time-dependent manner,inhibited migration in a time-dependent manner,and induced apoptosis in a dose-dependent manner in vitro;it also inhibited tumor growth in vivo.AKBA up-regulated the expression of PTEN and Bax,and downregulated the expression of proliferating cell nuclear antigen,Bcl-2,p-Akt,and COX-2 in a dose-dependent manner.The PTEN inhibitor bpv(Hopic)reversed the high expression of PTEN and low expression of p-Akt and COX-2 that were induced by AKBA.The Akt inhibitor MK2206 combined with AKBA downregulated the expression of p-Akt and COX-2,and the combined effect was better than that of AKBA alone.CONCLUSION AKBA inhibits the proliferation and migration and promotes the apoptosis of gastric cancer cells through the PTEN/Akt/COX-2 signaling pathway.展开更多
This study examined the effect of silencing LRIG3 expression on the proliferation and apoptosis of bladder cancer T24 cells and explored the role of LRIG3 in the tumorigenesis of bladder cancer. Bladder cancer T24 cel...This study examined the effect of silencing LRIG3 expression on the proliferation and apoptosis of bladder cancer T24 cells and explored the role of LRIG3 in the tumorigenesis of bladder cancer. Bladder cancer T24 cells were routinely cultured and pSilencer plasmids were employed to construct LRIG3 eukaryotic expression vector of LRIG3-siRNA, i.e., pSilencer-LRIG3-siRNA. After confirmation, the vector was transfected into HEK293 cells to make a replication-deficient adenovirus, pAd-LRIG3-siRNA, which was then introduced into bladder cancer T24 cells. RT-PCR, Western- blotting were performed to detect the levels of LRIG3 mRNA and proteins. Cells number was determined by using MTT test. Hoechst33258 staining, transmission microscopy, flow cytometery were conducted to examine the cell apoptosis. Three groups included a blank control group, a negative control group （containing non-interfering plasmids） and a pAd-LRIG3-siRNA group. Our results showed that the recombinant pAd-LRIG3-siRNA was successfully transfected into the bladder cancer T24 cells. The siRNA formed by the transcription of the recombinant plasmids resulted in significantly reduced expressions of LRIG3 gene and protein and significantly decreased cell proliferation and growth in the pAd-LRIG3-siRNA group as compared with the control group （P0.01）. The siRNA also caused apoptotic changes of some cells, with the apoptosis rate being （17.69±0.75）%, which was significantly different from that of the control group （P0.01）. It was concluded that recombinant pAd-LRIG3-siRNA plasmids could effectively decrease the expression of LRIG3 mRNA and proteins and, to some extent, inhibit the proliferation and promote the apoptosis of bladder cancer T24 cells. Silencing LRIG3 gene might be a novel alternative for the treatment of bladder cancer.展开更多
BACKGROUND： Previous studies have reported that statins are less toxic to the human body and have greater antitumor activity; however, few studies have addressed the antitumor effect of statins combined with tumor ne...BACKGROUND： Previous studies have reported that statins are less toxic to the human body and have greater antitumor activity; however, few studies have addressed the antitumor effect of statins combined with tumor necrosis factor-related apoptosis inducing ligand （TRAIL）. OBJECTIVE： To explore the effect of TRAIL combined with mevastatin on the proliferation and apoptotic cell death of a human glioma cell line SWO-38, and to study its mechanism of action. DESIGN, TIME AND SETTING： An in vitro control experiment was performed at the Central Laboratory of the Third Hospital Affiliated to Sun Yat-sen University, between January and April 2009. MATERIALS： The human SWO-38 cell line was provided by Cell Research, Department of Animal Experimental Center of Sun Yat-sen University; human recombinant soluble TRAIL by R＆D, USA; and mevastatin by Sigma, USA. METHODS： SWO-38 cells were separately incubated in TRAIL （100, 200, 300, 400, and 500 tJg/L） and mevastatin （5, 10, 20, 30, and 40 pmol/L） for 72 hours. In addition, SWO-38 cells were incubated in TRAIL （300 μg/L）, mevastatin （30 μmol/L）, and a solution containing both TRAIL and mevastatin for 12, 24, 48 and 72 hours. MAIN OUTCOME MEASURES： Cell proliferation was detected using methyl thiazolyl tetrazolium assay; cell apoptosis was observed using Hoechst 33258 staining and fluorescence microscopy and was measured using Annexin V/propidium iodide flow cytometry; TRAIL R1/DR4 and TRAIL R2/DR5 protein expressions levels were measured using indirect immunofluorescence staining combined with flow cytometry in the recombinant soluble TRAIL （rsTRAIL, 300 tJg/L）, mevastatin （30 IJmol/L） and combination groups; TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression was detected using real-time polymerase chain reaction. RESULTS： rsTRAIL, mevastatin and their combination inhibited tumor proliferation in a time- and dose-dependent manner. The proliferation inhibitory rate and apoptosis rate of human SWO-38 cells in the combined group were significantly greater than the rsTRAIL or mevastatin alone group （P 〈 0.01）. TRAIL R1/DR4 and TRAIL R2/DR5 protein and mRNA expressions were increased in the combination group compared with mevastatin or rsTRAIL alone after 72 hours （P 〈 0.01）. CONCLUSION： Both rsTRAIL and mevastatin inhibit the proliferation and apoptosis of the human glioma cell line SWO-38, while their combination enhances the anti-tumor effect. The mechanism of action possibly correlates to the upregulation of TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression by mevastatin, thereby enhancing the cell sensitivity to rsTRAIL.展开更多
Apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) can be regulated by the epidermal growth factor(EGF) signaling pathway.In this study,recombinant adenoviral vectors that encode TRAIL...Apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) can be regulated by the epidermal growth factor(EGF) signaling pathway.In this study,recombinant adenoviral vectors that encode TRAIL gene from the hTERT/RGD promoter(AdTRAIL) was combined with drugs including gefitinib,elotinib,and cetuximab that inhibit EGFR and the EGF signaling pathway in non-small cell lung cancer(NSCLC) cell lines to investigate their antitumor activity.In vitro,compared to single reagent,AdTRAIL combined with EGFR inhibitors reduced proliferation and enhanced apoptosis in H460,A549,and SW1573 cell lines.Western blot results suggested that these effects were relative to up-regulation of pro-apoptosis protein BAX and down-regulation of p-AKT.In vivo,AdTRAIL combined with cetuximab resulted in a significant growth reduction in H460 xenografts without damage to the main organs of nude mice.Histological examination and TUNEL analyses of xenografts showed that cetuximab enhanced cell apoptosis induced by AdTRAIL.These results indicate that EGFR inhibitors enhanced AdTRAIL anti-tumor activity in NSCLC cell lines and that inhibiting the AKT pathway played an important role in this enhancement.展开更多
AIM: There are conflicting data about p53 function on cellular sensitivity to the cytotoxic action of 5-fluorouracil (5-FU).Therefore the objective of this study was to determine the combined effects of adenovirus-med...AIM: There are conflicting data about p53 function on cellular sensitivity to the cytotoxic action of 5-fluorouracil (5-FU).Therefore the objective of this study was to determine the combined effects of adenovirus-mediated wild-type (wt) p53 gene transfer and 5-FU chemotherapy on pancreatic cancer cells with different p53 gene status.METHODS: Human pancreatic cancer cell lines Capan-1^p53mut,Capan-2^p53wt, FAMPAC^p53mut, PANG1^p53mut, and rat pancreatic cancer cell lines AS^p53wt and DSL6A^p53null were used for in vitro studies. Following infection with different ratios of Adp53-particles (MOI) in combination with 5-FU, proliferation of tumor cells and apoptosis were quantified by cell proliferation assay (WST-1) and FACS (PI-staining). In addition, DSL6A syngeneic pancreatic tumor cells were inoculated subcutaneously in to Lewis rats for in vivostudies.Tumor size, apoptosis (TUNEL) and survival were determined.RESULTS: Ad-p53 gene transfer combined with 5-FU significantly inhibited tumor cell proliferation and substantially enhanced apoptosis in all four cell lines with an alteration in the p53 gene compared to those two cell lines containing wt-p53. In vivo experiments showed the most effective tumor regression in animals treated with Ad-p53 plus 5-FU. Both in vitroand in vivoanalyses revealed that a sublethal dose of Ad-p53 augmented the apoptotic response induced by 5-FU.CONCLUSION: Our results suggest that Ad-p53 may synergistically enhance 5-FU-chemosensitivity most strikingly in pancreatic cancer cells lacking p53 function. These findings illustrate that the anticancer efficacy of this combination treatment is dependent on the p53 gene status of the target tumor cells.展开更多
Photodynamic therapy(PDT)has attracted much attention because of its advantages over chemotherapy,such as broad spectrum,high selectivity,and low drug resistance.However,most photosensitizers(PSs)used in PDT are O_(2)...Photodynamic therapy(PDT)has attracted much attention because of its advantages over chemotherapy,such as broad spectrum,high selectivity,and low drug resistance.However,most photosensitizers(PSs)used in PDT are O_(2)-dependent and show limited therapeutic efficacy toward hypoxic solid tumors.Therefore,developing PSs that produce reactive oxygen species(ROS)in an O_(2)-independent manner is highly demanded.Herein,we constructed a novel O_(2)-independent PS(TPA-N)based onα-diazo-aryl acetate,which could generate reactive carbene under visible light irradiation.Photoinduced carbene could react with biosubstrates and cause significant carbene stress and ROS,effectively killing tumor cells even under hypoxic conditions.TPA-N showed much less O_(2)dependence compared with traditional PDT reagent protoporphyrin IX.A mechanistic study suggested that TPAN could induce mitochondrial membrane potential collapse and upregulate apoptosis-related proteins upon light irradiation.This work provided a reliable strategy for developing O_(2)-independent PSs against hypoxic tumor cells through photoinduced carbene.展开更多
INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 a...INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer .展开更多
Cryptotanshinone is a natural active ingredient extracted from traditional Chinese medicine Radix Salviae Miltiorrhizae.It has a variety of pharmacological effects,in addition to preventing and treating ischemic disea...Cryptotanshinone is a natural active ingredient extracted from traditional Chinese medicine Radix Salviae Miltiorrhizae.It has a variety of pharmacological effects,in addition to preventing and treating ischemic diseases,coronary artery disease Alzheimer's disease and fighting tumors.The anti-tumor effects are exerted through inhibiting tumor cell proliferation,inducing tumor cell apoptosis,inhibiting tumor metastasis and invasion,inhibiting angiogenesis and regulating reactive oxygen species levels.The studies on the anti-tumor activity and action mechanism of cryptotanshinone in recent years are reviewed in this article.展开更多
Isoorientin can play an anti-tumor effect through interfering with tumor cell proliferation, inducing tumor cell apoptosis, regulating reactive oxygen species level, inducing tumor cell autophagy, blocking tumor cell ...Isoorientin can play an anti-tumor effect through interfering with tumor cell proliferation, inducing tumor cell apoptosis, regulating reactive oxygen species level, inducing tumor cell autophagy, blocking tumor cell infiltration and metastasis, inhibiting tumor neovascularization and other pathways. This paper reviews the research progress of anti-tumor activity and mechanism of isoorientin in recent years.展开更多
基金Supported by the Natural Science Foundation of Jiangsu,No.BK20171508。
文摘BACKGROUND Gastric cancer is one of the most common malignant tumors of the digestive system worldwide,posing a serious danger to human health.Cyclooxygenase(COX)-2 plays an important role in the carcinogenesis and progression of gastric cancer.Acetyl-11-keto-β-boswellic acid(AKBA)is a promising drug for cancer therapy,but its effects and mechanism of action on human gastric cancer remain unclear.AIM To evaluate whether the phosphatase and tensin homolog(PTEN)/Akt/COX-2 signaling pathway is involved in the anti-tumor effect of AKBA in gastric cancer.METHODS Human poorly differentiated BGC823 and moderately differentiated SGC7901 gastric cancer cells were routinely cultured in Roswell Park Memorial Institute 1640 medium supplemented with 10%fetal bovine serum and 1%penicillin/streptomycin.Gastric cancer cell proliferation was determined by methyl thiazolyl tetrazolium colorimetric assay.Apoptosis was measured by flow cytometry.Cell migration was assessed using the wound-healing assay.Expression of Bcl-2,Bax,proliferating cell nuclear antigen,PTEN,p-Akt,and COX-2 were detected by Western blot analysis.A xenograft nude mouse model of human gastric cancer was established to evaluate the anti-cancer effect of AKBA RESULTS AKBA significantly inhibited the proliferation of gastric cancer cells in a dose-and time-dependent manner,inhibited migration in a time-dependent manner,and induced apoptosis in a dose-dependent manner in vitro;it also inhibited tumor growth in vivo.AKBA up-regulated the expression of PTEN and Bax,and downregulated the expression of proliferating cell nuclear antigen,Bcl-2,p-Akt,and COX-2 in a dose-dependent manner.The PTEN inhibitor bpv(Hopic)reversed the high expression of PTEN and low expression of p-Akt and COX-2 that were induced by AKBA.The Akt inhibitor MK2206 combined with AKBA downregulated the expression of p-Akt and COX-2,and the combined effect was better than that of AKBA alone.CONCLUSION AKBA inhibits the proliferation and migration and promotes the apoptosis of gastric cancer cells through the PTEN/Akt/COX-2 signaling pathway.
基金supported by a grant from Hubei Provincial Natural Sciences Foundation (No. 2004ABA-205)
文摘This study examined the effect of silencing LRIG3 expression on the proliferation and apoptosis of bladder cancer T24 cells and explored the role of LRIG3 in the tumorigenesis of bladder cancer. Bladder cancer T24 cells were routinely cultured and pSilencer plasmids were employed to construct LRIG3 eukaryotic expression vector of LRIG3-siRNA, i.e., pSilencer-LRIG3-siRNA. After confirmation, the vector was transfected into HEK293 cells to make a replication-deficient adenovirus, pAd-LRIG3-siRNA, which was then introduced into bladder cancer T24 cells. RT-PCR, Western- blotting were performed to detect the levels of LRIG3 mRNA and proteins. Cells number was determined by using MTT test. Hoechst33258 staining, transmission microscopy, flow cytometery were conducted to examine the cell apoptosis. Three groups included a blank control group, a negative control group （containing non-interfering plasmids） and a pAd-LRIG3-siRNA group. Our results showed that the recombinant pAd-LRIG3-siRNA was successfully transfected into the bladder cancer T24 cells. The siRNA formed by the transcription of the recombinant plasmids resulted in significantly reduced expressions of LRIG3 gene and protein and significantly decreased cell proliferation and growth in the pAd-LRIG3-siRNA group as compared with the control group （P0.01）. The siRNA also caused apoptotic changes of some cells, with the apoptosis rate being （17.69±0.75）%, which was significantly different from that of the control group （P0.01）. It was concluded that recombinant pAd-LRIG3-siRNA plasmids could effectively decrease the expression of LRIG3 mRNA and proteins and, to some extent, inhibit the proliferation and promote the apoptosis of bladder cancer T24 cells. Silencing LRIG3 gene might be a novel alternative for the treatment of bladder cancer.
基金the National Natural Science Foundation of China, No. 30772537
文摘BACKGROUND： Previous studies have reported that statins are less toxic to the human body and have greater antitumor activity; however, few studies have addressed the antitumor effect of statins combined with tumor necrosis factor-related apoptosis inducing ligand （TRAIL）. OBJECTIVE： To explore the effect of TRAIL combined with mevastatin on the proliferation and apoptotic cell death of a human glioma cell line SWO-38, and to study its mechanism of action. DESIGN, TIME AND SETTING： An in vitro control experiment was performed at the Central Laboratory of the Third Hospital Affiliated to Sun Yat-sen University, between January and April 2009. MATERIALS： The human SWO-38 cell line was provided by Cell Research, Department of Animal Experimental Center of Sun Yat-sen University; human recombinant soluble TRAIL by R＆D, USA; and mevastatin by Sigma, USA. METHODS： SWO-38 cells were separately incubated in TRAIL （100, 200, 300, 400, and 500 tJg/L） and mevastatin （5, 10, 20, 30, and 40 pmol/L） for 72 hours. In addition, SWO-38 cells were incubated in TRAIL （300 μg/L）, mevastatin （30 μmol/L）, and a solution containing both TRAIL and mevastatin for 12, 24, 48 and 72 hours. MAIN OUTCOME MEASURES： Cell proliferation was detected using methyl thiazolyl tetrazolium assay; cell apoptosis was observed using Hoechst 33258 staining and fluorescence microscopy and was measured using Annexin V/propidium iodide flow cytometry; TRAIL R1/DR4 and TRAIL R2/DR5 protein expressions levels were measured using indirect immunofluorescence staining combined with flow cytometry in the recombinant soluble TRAIL （rsTRAIL, 300 tJg/L）, mevastatin （30 IJmol/L） and combination groups; TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression was detected using real-time polymerase chain reaction. RESULTS： rsTRAIL, mevastatin and their combination inhibited tumor proliferation in a time- and dose-dependent manner. The proliferation inhibitory rate and apoptosis rate of human SWO-38 cells in the combined group were significantly greater than the rsTRAIL or mevastatin alone group （P 〈 0.01）. TRAIL R1/DR4 and TRAIL R2/DR5 protein and mRNA expressions were increased in the combination group compared with mevastatin or rsTRAIL alone after 72 hours （P 〈 0.01）. CONCLUSION： Both rsTRAIL and mevastatin inhibit the proliferation and apoptosis of the human glioma cell line SWO-38, while their combination enhances the anti-tumor effect. The mechanism of action possibly correlates to the upregulation of TRAIL R1/DR4 and TRAIL R2/DR5 mRNA expression by mevastatin, thereby enhancing the cell sensitivity to rsTRAIL.
文摘Apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) can be regulated by the epidermal growth factor(EGF) signaling pathway.In this study,recombinant adenoviral vectors that encode TRAIL gene from the hTERT/RGD promoter(AdTRAIL) was combined with drugs including gefitinib,elotinib,and cetuximab that inhibit EGFR and the EGF signaling pathway in non-small cell lung cancer(NSCLC) cell lines to investigate their antitumor activity.In vitro,compared to single reagent,AdTRAIL combined with EGFR inhibitors reduced proliferation and enhanced apoptosis in H460,A549,and SW1573 cell lines.Western blot results suggested that these effects were relative to up-regulation of pro-apoptosis protein BAX and down-regulation of p-AKT.In vivo,AdTRAIL combined with cetuximab resulted in a significant growth reduction in H460 xenografts without damage to the main organs of nude mice.Histological examination and TUNEL analyses of xenografts showed that cetuximab enhanced cell apoptosis induced by AdTRAIL.These results indicate that EGFR inhibitors enhanced AdTRAIL anti-tumor activity in NSCLC cell lines and that inhibiting the AKT pathway played an important role in this enhancement.
文摘AIM: There are conflicting data about p53 function on cellular sensitivity to the cytotoxic action of 5-fluorouracil (5-FU).Therefore the objective of this study was to determine the combined effects of adenovirus-mediated wild-type (wt) p53 gene transfer and 5-FU chemotherapy on pancreatic cancer cells with different p53 gene status.METHODS: Human pancreatic cancer cell lines Capan-1^p53mut,Capan-2^p53wt, FAMPAC^p53mut, PANG1^p53mut, and rat pancreatic cancer cell lines AS^p53wt and DSL6A^p53null were used for in vitro studies. Following infection with different ratios of Adp53-particles (MOI) in combination with 5-FU, proliferation of tumor cells and apoptosis were quantified by cell proliferation assay (WST-1) and FACS (PI-staining). In addition, DSL6A syngeneic pancreatic tumor cells were inoculated subcutaneously in to Lewis rats for in vivostudies.Tumor size, apoptosis (TUNEL) and survival were determined.RESULTS: Ad-p53 gene transfer combined with 5-FU significantly inhibited tumor cell proliferation and substantially enhanced apoptosis in all four cell lines with an alteration in the p53 gene compared to those two cell lines containing wt-p53. In vivo experiments showed the most effective tumor regression in animals treated with Ad-p53 plus 5-FU. Both in vitroand in vivoanalyses revealed that a sublethal dose of Ad-p53 augmented the apoptotic response induced by 5-FU.CONCLUSION: Our results suggest that Ad-p53 may synergistically enhance 5-FU-chemosensitivity most strikingly in pancreatic cancer cells lacking p53 function. These findings illustrate that the anticancer efficacy of this combination treatment is dependent on the p53 gene status of the target tumor cells.
基金financial support from the National Natural Science Foundation of China(grant nos.22122701,21977044,21731004,91953201,92153303,and 21907050)the Natural Science Foundation of Jiangsu Province(grant no.BK20202004)+1 种基金the Excellent Research Program of Nanjing University(grant no.ZYJH004)the Open Research Fund of the National Center for Protein Sciences at Peking University in Beijing(grant no.KF-202201).
文摘Photodynamic therapy(PDT)has attracted much attention because of its advantages over chemotherapy,such as broad spectrum,high selectivity,and low drug resistance.However,most photosensitizers(PSs)used in PDT are O_(2)-dependent and show limited therapeutic efficacy toward hypoxic solid tumors.Therefore,developing PSs that produce reactive oxygen species(ROS)in an O_(2)-independent manner is highly demanded.Herein,we constructed a novel O_(2)-independent PS(TPA-N)based onα-diazo-aryl acetate,which could generate reactive carbene under visible light irradiation.Photoinduced carbene could react with biosubstrates and cause significant carbene stress and ROS,effectively killing tumor cells even under hypoxic conditions.TPA-N showed much less O_(2)dependence compared with traditional PDT reagent protoporphyrin IX.A mechanistic study suggested that TPAN could induce mitochondrial membrane potential collapse and upregulate apoptosis-related proteins upon light irradiation.This work provided a reliable strategy for developing O_(2)-independent PSs against hypoxic tumor cells through photoinduced carbene.
基金Supported by the Medical Research Foundation of Guangdong Province,No.1997423
文摘INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer .
基金Supported by Multigrain Production and Processing Characteristic Discipline Construction ProjectPostdoctoral Scientific Research Foundation of Heilongjiang Province of China(LBH-Q13132)
文摘Cryptotanshinone is a natural active ingredient extracted from traditional Chinese medicine Radix Salviae Miltiorrhizae.It has a variety of pharmacological effects,in addition to preventing and treating ischemic diseases,coronary artery disease Alzheimer's disease and fighting tumors.The anti-tumor effects are exerted through inhibiting tumor cell proliferation,inducing tumor cell apoptosis,inhibiting tumor metastasis and invasion,inhibiting angiogenesis and regulating reactive oxygen species levels.The studies on the anti-tumor activity and action mechanism of cryptotanshinone in recent years are reviewed in this article.
基金Supported by Multigrain Production and Processing Characteristic Discipline Construction ProjectPostdoctoral Scientific Research Foundation of Heilongjiang Province of China(LBH-Q13132)National Key Research and Development Plan"Regulation and Activity Retention Technology and Application of Coarse Cereals Active Components in Processing"(2017YFD0401203)
文摘Isoorientin can play an anti-tumor effect through interfering with tumor cell proliferation, inducing tumor cell apoptosis, regulating reactive oxygen species level, inducing tumor cell autophagy, blocking tumor cell infiltration and metastasis, inhibiting tumor neovascularization and other pathways. This paper reviews the research progress of anti-tumor activity and mechanism of isoorientin in recent years.
