Objective: To investigate the effects of histamine on growth and apoptosis of human melanoma cells A375. Methods: The effect of histamine on growth of A375 cells in vitro was examined by MTT assay and Trypan blue excl...Objective: To investigate the effects of histamine on growth and apoptosis of human melanoma cells A375. Methods: The effect of histamine on growth of A375 cells in vitro was examined by MTT assay and Trypan blue exclusion assay. Cell cycle analysis, early apoptosis analysis by double staining with Annexin V-FITC and PI, and active caspase-3 analysis by staining FITC-conjugated monoclonal rabbit anti-active caspase-3 antibody were made by flow cytometer. StreptAvidin-Biotin Complex (SABC) immunocytochemical assays were adopted to detect Bax/Bcl-2 protein expressions.Results: Histamine inhibited proliferation of A375 cells in a dose- and time-dependent manner, and altered cell cycle distribution of A375 cells revealing an increase in G0/G1-phase population, a decrease in S-phase population and the inhibition of G1/S switching. Histamine induced apoptosis of A375 cells (P<0.05), elevated the cells population with detectable active caspase-3 (P<0.05), increased the number of cells forming Bax and decreased the number of cells forming Bcl-2 significantly (P<0.05). Conclusion: That histamine inhibits cell cycle progress of A375 cells is one of the possible mechanisms of proliferation arrest of A375 cells elicited by histamine. Histamine mediates apoptosis in A375 cells that may be caspase-dependent through mitochondria routine. Histamine with high concentration inhibits growth of A375 cells in vitro by interfering proliferation and inducing apoptosis of cells.展开更多
[Objectives] The aim was to investigate the effect of cryptotanshinone on apoptosis of human melanoma A375 cells and its related mechanism of mitochondrial pathway.[Methods]The cytotoxic effect of cryptotanshinone on ...[Objectives] The aim was to investigate the effect of cryptotanshinone on apoptosis of human melanoma A375 cells and its related mechanism of mitochondrial pathway.[Methods]The cytotoxic effect of cryptotanshinone on apoptosis of human melanoma A375 cells was detected by MTT colorimetry.The apoptosis of melanoma A375 cells was detected with Annexin V-FITC/PI and observed by fluorescence inverted microscope.The expression of apoptosis-related proteins was detected by Western blotting.[Results]The viability of the A375 cells decreased with the increase of drug concentration.The fluorescence intensity of the cells increased with the treatment time.The expression of pro-apoptotic protein caspase-3 gradually increased,while the expression of apoptosis-inhibiting proteins p-AKT and Bcl-2 gradually reduced.[Conclusions]Cryptotanshinone induces apoptosis of human melanoma A375 cells via AKT signaling pathway,thus exerting a good cytotoxic effect on A375 cells.展开更多
Objective: he effect of M3 receptor antagonist 4-DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) on the proliferation of melanoma were explored, and the development prospect and significance of M3 receptor anta...Objective: he effect of M3 receptor antagonist 4-DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) on the proliferation of melanoma were explored, and the development prospect and significance of M3 receptor antagonist in the field of anti-tumor were discussed. Methods: The viability of tumor cells was detected by MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) colorimetry. The optimal concentration of 4-DAMP was screened and the effect of the drug was confirmed by EdU (5-ethynyl-2'-deoxyuridine) fluorescence staining. Adult male BALB/c nude mice were divided into control group, 5-Fu (5-Fluorouracil, 5-Fluorouracil, 20 mg/kg/d) group and 4-DAMP (2 mg/kg/d) group to establishtumor-bearing model in vivo. The tumor volume curve was calculated and plotted. Mice were killed after 21 days of continuous administration. Strip the tumor, take pictures and meatured the weighs, and calculate the inhibition rate. [1]The spleen was weighed and the spleen index was culculated. H & E staining was used to observe the pathological changes of tumor sections. The gene expression of M3R、MIA (Melanoma inhibitory activity, MIA)、SP-1 (Transcription factor Sp1, SP-1) and Lnc-SPRY4-IT1 (SPRY4 Intronic Transcript 1,Lnc-SPRY4-IT1) in A375 cell line was detected by real-time quantitative PCR (quantitative reverse-transcription polymerase chain reaction, qRT-PCR). The protein level of ERK1/2 (extracellular signal-regulated kinase 1/2,ERK1/2) was detected by Western Blot. Results: 4-DAMP could significantly inhibit the activity of A375 cell line (P < 0.01), and EdU staining demonstrated that 4-DAMP inhibited the growth of A375 cell line. The results of animal experiments showed that compared with the control group, the volume and mass of tumor in 5-Fu group and 4-DAMP group were significantly reduced (P < 0.05) and H & E staining showed that the intercellular space became larger, connective tissue increased, and tumor growth was obstructed. Compared with the control group, the tumor inhibition rate of 4-DAMP group was 72.01% (P < 0.01). There was no significant difference in body mass and spleen index. Compared with the control group, the expression of MIA, SP-1 and LncRNA-SPRY4-IT1 was decreased by 4-DAMP or si-M3R transfection. Compared with the control group, the expression of ERK1/2 was decreased by 4-DAMP or si-M3R transfection. Conclusions: These results suggest that M3 receptor antagonist 4-DAMP can inhibit the proliferation of melanoma and reduce the expression of mRNA of MIA, SP-1 and LncRNA-SPRY4-IT1 and the protein level of ERK1/2 in A375 tumor cells.展开更多
Objective:To estimate electroporation(EP) influence on malignant and normal cells.Methods: Two cell lines including human malignant melanoma(Me-43) and normal human gingival fibroblast(HCFs) were used.EP parameters we...Objective:To estimate electroporation(EP) influence on malignant and normal cells.Methods: Two cell lines including human malignant melanoma(Me-43) and normal human gingival fibroblast(HCFs) were used.EP parameters were the following:230,1000,1 730,2 300 V/cm;30 μ s by 3 impulses for every case.The viability of cells after EP was estimated by MTT assay. The ullrastructural analysis was observed by transmission electron microscope(Zeiss EM 900). Results:In the current study we observed the intracellular effect following EP on Me-43 and HGF cells.At the conditions applied,we did not observe any significant damage of mitochondrial activity in both cell lines treated by EP.Conversely,we showed that EP in some conditions can stimulate cells to proliferation.Some changes induced by EP were only visible in electron microscopy.In fibroblast cells we observed significant changes in lower parameters of EP(230 and 1 000 V/cm).After applying higher electric field intensities(2 300 V/cm) we detected many vacuoles,myelin-like bodies and swallowed endoplasmic reticulum.In melanoma cells such strong pathological modifications after EP were not observed,in comparison with control cells. The ultrastructure of both treated cell lines was changed according to the applied parameters of EP.Conclusions:We can claim that EP conditions are cell line dependent.In terms of the intracellular morphology,human fibroblasts are more sensitive to electric field as compared with melanoma cells.Optimal conditions should be determined for each cell line.Summarizing our study,we can conclude that EP is not an invasive method for human normal and malignant cells. This technique can be safely applied in chemotherapy for delivering drugs into tumor cells.展开更多
AIM:To investigate the effects of luteolin on apoptosis,the cell cycle,and the expression and secretion of vascular endothelial growth factor(VEGF)in human choroidal melanoma cells(C918 and OCM-1).METHODS:C918 and OCM...AIM:To investigate the effects of luteolin on apoptosis,the cell cycle,and the expression and secretion of vascular endothelial growth factor(VEGF)in human choroidal melanoma cells(C918 and OCM-1).METHODS:C918 and OCM-1 cells cultured in vitro were treated with various concentrations of luteolin(0,5,10,15μmol/L).Cell growth was observed with an inverted microscope,and cell cycle arrest was detected by propidium iodide(PI)staining using flow cytometry.Apoptosis was detected by Hoechst33342 staining,and apoptosis rate was determined by Annexin V-FITC/PI experiments using flow cytometry.The expression of apoptosis-related proteins Bcl-2,Bax and VEGF was analyzed using Western blots.The levels of VEGF secreted by the cells into the supernatant was analyzed using ELISA.RESULTS:After treating with 5 to 15μmol/L luteolin for 48 h,the fusion degree of C918 and OCM-1 cells decreased,and more floating apoptotic cells appeared.Luteolin treatment increased the G0-G1 phase ratio of the C918 and OCM-1 cells,blocked cell cycle progression,and increased the apoptosis rate of the C918 and OCM-1 cells.Western blot showed that luteolin decreased the expression of Bcl-2 and VEGF in the C918 and OCM-1 cells and increased the expression of Bax protein.The ELISA results showed that 10 to 15μmol/L luteolin decreased the cell secretion of VEGF.CONCLUSION:Luteolin may induce apoptosis by regulating the levels of apoptosis-related proteins in C918 and OCM-1 cells.Luteolin can induce cell cycle arrest,decrease the expression of VEGF.展开更多
This study aimed to investigate the effects of celecoxib,synthetic retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalenecarboxylicacid(CD437)and the combination of the two on cell proliferation,apoptosis,and cycl...This study aimed to investigate the effects of celecoxib,synthetic retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalenecarboxylicacid(CD437)and the combination of the two on cell proliferation,apoptosis,and cycle arrest of human malignant mela-noma A375 cells.3-(4,5-dimethylthiazol-2-yl)-2,5-di-phenyltetrazoliumbromide assay(MTT assay)was applied to determine the anti-proliferative effects of the drugs on human malignant melanoma A375 cells.Flow cytometry was performed to investigate the influence of the drugs on cell cycle and cell apoptosis.Both celecoxib and CD437 could inhibit the growth of human malignant melanoma A375 cells in a dose-dependent manner.Celecoxib at 80μmol/L inhibited proliferation,induced apoptosis and G2/M cell cycle arrest of human malignant melanoma A375 cells after treatment for 24 h[proliferation inhibiting rate:(50.2±2.51)%,apoptosis rate:(35.91±1.80)%].CD437 at 10μmol/L inhibited proliferation,induced apoptosis and G0/G1 cell cycle arrest of human malignant melanoma A375 cells after treatment for 24 h[proliferation inhibiting rate:(58.6±2.38)%,apoptosis rate:(28.03±0.77)%].Celecoxib in combination with CD437 could significantly enhance the effects of inhibiting proliferation and inducing apoptosis of human malignant melanoma A375 cells 24 h after treatment compared with the drug alone[proliferation inhibiting rate:(68.92±1.72)%,apop-tosis rate:(42.09±1.05)%,both P<0.05]and decrease the proportion of the S phase in the cell cycle.Celecoxib could inhibit the growth of human malignant melanoma A375 cells by inducing apoptosis and G2/M cycle arrest.CD437 could inhibit the growth of human malignant melanoma A375 cells by inducing apoptosis and G0/G1 cycle arrest.Celecoxib exhibited additive effects with CD437 on retarding the growth and inducing apoptosis of human malignant melanoma A375 cells.Celecoxib in combination with CD437 may become an effective method for prevention and treatment of human melanoma.展开更多
Unique characteristics in fetal development include scar-less wound healing and the paucity of tumor formation. Recent studies have demonstrated that the embryonic microenvironment can reverse melanoma cells to a beni...Unique characteristics in fetal development include scar-less wound healing and the paucity of tumor formation. Recent studies have demonstrated that the embryonic microenvironment can reverse melanoma cells to a benign melanocyte phenotype. We bioengineered embryonic-like compositions and tested the anti-cancer activity of this material on a panel of skin cancer lines. To simulate the embryonic environment, neonatal fibroblasts were grown in hypoxic suspension cultures. The cells reverted back into multipotent stem cells as evidenced by the upregulation of SOX2, Oct4, NANOG, and KLF4 genes, and by the expression of stem cell-associated proteins including Nodal, Brachyury, Nestin, and Oct4. Cell Conditioned Media (CCM) and human Extracellular Matrix Proteins (hECM) produced by these cells were tested for their ability to reduce cell viability in skin cancer cell lines. In vitro studies with CCM and hECM show reduction in Squamous Cell Carcinoma (SCC), Basal Cell Carcinoma (BCC) and melanoma cell number through upregulation of caspases and induction of apoptosis. In the chick allantoic membrane assay, melanoma load was reduced by up to 80% with hECM treatment compared to vehicle treated controls (p 0.05). Similar inhibition was seen with SCC cells. In a xenograft mouse model of subcutaneous melanoma, tumor growth was inhibited by 70% - 90%. These data suggest that CCM and hECM have anti tumor potential and might offer a new treatment strategy in skin cancer.展开更多
RU-486 is an abortifacient which is used to terminate early pregnancy. It acts by blocking progesterone receptor. In our earlier study with progesterone, RU-486 was used as a progesterone receptor antagonist to find o...RU-486 is an abortifacient which is used to terminate early pregnancy. It acts by blocking progesterone receptor. In our earlier study with progesterone, RU-486 was used as a progesterone receptor antagonist to find out the mechanism of progesterone action on melanoma cells. Results indicated that the effect of progesterone was not mediated through progesterone receptor. In the course of experiments, it was observed that RU-486 by itself inhibited mouse melanoma cell growth. Further research work with RU-486 showed a dose dependent inhibition of human melanoma cell growth. The mechanism of inhibition of cell growth was due to apoptosis and this effect of RU-486 was neither mediated through progesterone receptor nor glucocorticoid receptor. This in-vitro study suggested that melanoma also could be a target for RU-486 action, apart from breast, ovary and prostate cancers.展开更多
文摘Objective: To investigate the effects of histamine on growth and apoptosis of human melanoma cells A375. Methods: The effect of histamine on growth of A375 cells in vitro was examined by MTT assay and Trypan blue exclusion assay. Cell cycle analysis, early apoptosis analysis by double staining with Annexin V-FITC and PI, and active caspase-3 analysis by staining FITC-conjugated monoclonal rabbit anti-active caspase-3 antibody were made by flow cytometer. StreptAvidin-Biotin Complex (SABC) immunocytochemical assays were adopted to detect Bax/Bcl-2 protein expressions.Results: Histamine inhibited proliferation of A375 cells in a dose- and time-dependent manner, and altered cell cycle distribution of A375 cells revealing an increase in G0/G1-phase population, a decrease in S-phase population and the inhibition of G1/S switching. Histamine induced apoptosis of A375 cells (P<0.05), elevated the cells population with detectable active caspase-3 (P<0.05), increased the number of cells forming Bax and decreased the number of cells forming Bcl-2 significantly (P<0.05). Conclusion: That histamine inhibits cell cycle progress of A375 cells is one of the possible mechanisms of proliferation arrest of A375 cells elicited by histamine. Histamine mediates apoptosis in A375 cells that may be caspase-dependent through mitochondria routine. Histamine with high concentration inhibits growth of A375 cells in vitro by interfering proliferation and inducing apoptosis of cells.
基金Supported by Multigrain Production and Processing Characteristic Discipline Construction ProjectPostdoctoral Scientific Research Foundation of Heilongjiang Province of China(LBH-Q13132)
文摘[Objectives] The aim was to investigate the effect of cryptotanshinone on apoptosis of human melanoma A375 cells and its related mechanism of mitochondrial pathway.[Methods]The cytotoxic effect of cryptotanshinone on apoptosis of human melanoma A375 cells was detected by MTT colorimetry.The apoptosis of melanoma A375 cells was detected with Annexin V-FITC/PI and observed by fluorescence inverted microscope.The expression of apoptosis-related proteins was detected by Western blotting.[Results]The viability of the A375 cells decreased with the increase of drug concentration.The fluorescence intensity of the cells increased with the treatment time.The expression of pro-apoptotic protein caspase-3 gradually increased,while the expression of apoptosis-inhibiting proteins p-AKT and Bcl-2 gradually reduced.[Conclusions]Cryptotanshinone induces apoptosis of human melanoma A375 cells via AKT signaling pathway,thus exerting a good cytotoxic effect on A375 cells.
基金High-level Talents Fund of Natural Science Foundation of Hainan Province(No.2019RC376).
文摘Objective: he effect of M3 receptor antagonist 4-DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) on the proliferation of melanoma were explored, and the development prospect and significance of M3 receptor antagonist in the field of anti-tumor were discussed. Methods: The viability of tumor cells was detected by MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) colorimetry. The optimal concentration of 4-DAMP was screened and the effect of the drug was confirmed by EdU (5-ethynyl-2'-deoxyuridine) fluorescence staining. Adult male BALB/c nude mice were divided into control group, 5-Fu (5-Fluorouracil, 5-Fluorouracil, 20 mg/kg/d) group and 4-DAMP (2 mg/kg/d) group to establishtumor-bearing model in vivo. The tumor volume curve was calculated and plotted. Mice were killed after 21 days of continuous administration. Strip the tumor, take pictures and meatured the weighs, and calculate the inhibition rate. [1]The spleen was weighed and the spleen index was culculated. H & E staining was used to observe the pathological changes of tumor sections. The gene expression of M3R、MIA (Melanoma inhibitory activity, MIA)、SP-1 (Transcription factor Sp1, SP-1) and Lnc-SPRY4-IT1 (SPRY4 Intronic Transcript 1,Lnc-SPRY4-IT1) in A375 cell line was detected by real-time quantitative PCR (quantitative reverse-transcription polymerase chain reaction, qRT-PCR). The protein level of ERK1/2 (extracellular signal-regulated kinase 1/2,ERK1/2) was detected by Western Blot. Results: 4-DAMP could significantly inhibit the activity of A375 cell line (P < 0.01), and EdU staining demonstrated that 4-DAMP inhibited the growth of A375 cell line. The results of animal experiments showed that compared with the control group, the volume and mass of tumor in 5-Fu group and 4-DAMP group were significantly reduced (P < 0.05) and H & E staining showed that the intercellular space became larger, connective tissue increased, and tumor growth was obstructed. Compared with the control group, the tumor inhibition rate of 4-DAMP group was 72.01% (P < 0.01). There was no significant difference in body mass and spleen index. Compared with the control group, the expression of MIA, SP-1 and LncRNA-SPRY4-IT1 was decreased by 4-DAMP or si-M3R transfection. Compared with the control group, the expression of ERK1/2 was decreased by 4-DAMP or si-M3R transfection. Conclusions: These results suggest that M3 receptor antagonist 4-DAMP can inhibit the proliferation of melanoma and reduce the expression of mRNA of MIA, SP-1 and LncRNA-SPRY4-IT1 and the protein level of ERK1/2 in A375 tumor cells.
基金Suppoted by statutory funds of Medical Wroelaw University andresearch Tellowship within"Development Program of Wroclaw Medical University"funded from European Social Fund.Human CapitalNational Cohesion Strategy(Contract No.UDA-POKL.04.01.01-00-010/08-00)
文摘Objective:To estimate electroporation(EP) influence on malignant and normal cells.Methods: Two cell lines including human malignant melanoma(Me-43) and normal human gingival fibroblast(HCFs) were used.EP parameters were the following:230,1000,1 730,2 300 V/cm;30 μ s by 3 impulses for every case.The viability of cells after EP was estimated by MTT assay. The ullrastructural analysis was observed by transmission electron microscope(Zeiss EM 900). Results:In the current study we observed the intracellular effect following EP on Me-43 and HGF cells.At the conditions applied,we did not observe any significant damage of mitochondrial activity in both cell lines treated by EP.Conversely,we showed that EP in some conditions can stimulate cells to proliferation.Some changes induced by EP were only visible in electron microscopy.In fibroblast cells we observed significant changes in lower parameters of EP(230 and 1 000 V/cm).After applying higher electric field intensities(2 300 V/cm) we detected many vacuoles,myelin-like bodies and swallowed endoplasmic reticulum.In melanoma cells such strong pathological modifications after EP were not observed,in comparison with control cells. The ultrastructure of both treated cell lines was changed according to the applied parameters of EP.Conclusions:We can claim that EP conditions are cell line dependent.In terms of the intracellular morphology,human fibroblasts are more sensitive to electric field as compared with melanoma cells.Optimal conditions should be determined for each cell line.Summarizing our study,we can conclude that EP is not an invasive method for human normal and malignant cells. This technique can be safely applied in chemotherapy for delivering drugs into tumor cells.
文摘AIM:To investigate the effects of luteolin on apoptosis,the cell cycle,and the expression and secretion of vascular endothelial growth factor(VEGF)in human choroidal melanoma cells(C918 and OCM-1).METHODS:C918 and OCM-1 cells cultured in vitro were treated with various concentrations of luteolin(0,5,10,15μmol/L).Cell growth was observed with an inverted microscope,and cell cycle arrest was detected by propidium iodide(PI)staining using flow cytometry.Apoptosis was detected by Hoechst33342 staining,and apoptosis rate was determined by Annexin V-FITC/PI experiments using flow cytometry.The expression of apoptosis-related proteins Bcl-2,Bax and VEGF was analyzed using Western blots.The levels of VEGF secreted by the cells into the supernatant was analyzed using ELISA.RESULTS:After treating with 5 to 15μmol/L luteolin for 48 h,the fusion degree of C918 and OCM-1 cells decreased,and more floating apoptotic cells appeared.Luteolin treatment increased the G0-G1 phase ratio of the C918 and OCM-1 cells,blocked cell cycle progression,and increased the apoptosis rate of the C918 and OCM-1 cells.Western blot showed that luteolin decreased the expression of Bcl-2 and VEGF in the C918 and OCM-1 cells and increased the expression of Bax protein.The ELISA results showed that 10 to 15μmol/L luteolin decreased the cell secretion of VEGF.CONCLUSION:Luteolin may induce apoptosis by regulating the levels of apoptosis-related proteins in C918 and OCM-1 cells.Luteolin can induce cell cycle arrest,decrease the expression of VEGF.
基金supported by the National Natural Science Foundation of China(Grant No.30371295).
文摘This study aimed to investigate the effects of celecoxib,synthetic retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalenecarboxylicacid(CD437)and the combination of the two on cell proliferation,apoptosis,and cycle arrest of human malignant mela-noma A375 cells.3-(4,5-dimethylthiazol-2-yl)-2,5-di-phenyltetrazoliumbromide assay(MTT assay)was applied to determine the anti-proliferative effects of the drugs on human malignant melanoma A375 cells.Flow cytometry was performed to investigate the influence of the drugs on cell cycle and cell apoptosis.Both celecoxib and CD437 could inhibit the growth of human malignant melanoma A375 cells in a dose-dependent manner.Celecoxib at 80μmol/L inhibited proliferation,induced apoptosis and G2/M cell cycle arrest of human malignant melanoma A375 cells after treatment for 24 h[proliferation inhibiting rate:(50.2±2.51)%,apoptosis rate:(35.91±1.80)%].CD437 at 10μmol/L inhibited proliferation,induced apoptosis and G0/G1 cell cycle arrest of human malignant melanoma A375 cells after treatment for 24 h[proliferation inhibiting rate:(58.6±2.38)%,apoptosis rate:(28.03±0.77)%].Celecoxib in combination with CD437 could significantly enhance the effects of inhibiting proliferation and inducing apoptosis of human malignant melanoma A375 cells 24 h after treatment compared with the drug alone[proliferation inhibiting rate:(68.92±1.72)%,apop-tosis rate:(42.09±1.05)%,both P<0.05]and decrease the proportion of the S phase in the cell cycle.Celecoxib could inhibit the growth of human malignant melanoma A375 cells by inducing apoptosis and G2/M cycle arrest.CD437 could inhibit the growth of human malignant melanoma A375 cells by inducing apoptosis and G0/G1 cycle arrest.Celecoxib exhibited additive effects with CD437 on retarding the growth and inducing apoptosis of human malignant melanoma A375 cells.Celecoxib in combination with CD437 may become an effective method for prevention and treatment of human melanoma.
文摘Unique characteristics in fetal development include scar-less wound healing and the paucity of tumor formation. Recent studies have demonstrated that the embryonic microenvironment can reverse melanoma cells to a benign melanocyte phenotype. We bioengineered embryonic-like compositions and tested the anti-cancer activity of this material on a panel of skin cancer lines. To simulate the embryonic environment, neonatal fibroblasts were grown in hypoxic suspension cultures. The cells reverted back into multipotent stem cells as evidenced by the upregulation of SOX2, Oct4, NANOG, and KLF4 genes, and by the expression of stem cell-associated proteins including Nodal, Brachyury, Nestin, and Oct4. Cell Conditioned Media (CCM) and human Extracellular Matrix Proteins (hECM) produced by these cells were tested for their ability to reduce cell viability in skin cancer cell lines. In vitro studies with CCM and hECM show reduction in Squamous Cell Carcinoma (SCC), Basal Cell Carcinoma (BCC) and melanoma cell number through upregulation of caspases and induction of apoptosis. In the chick allantoic membrane assay, melanoma load was reduced by up to 80% with hECM treatment compared to vehicle treated controls (p 0.05). Similar inhibition was seen with SCC cells. In a xenograft mouse model of subcutaneous melanoma, tumor growth was inhibited by 70% - 90%. These data suggest that CCM and hECM have anti tumor potential and might offer a new treatment strategy in skin cancer.
文摘RU-486 is an abortifacient which is used to terminate early pregnancy. It acts by blocking progesterone receptor. In our earlier study with progesterone, RU-486 was used as a progesterone receptor antagonist to find out the mechanism of progesterone action on melanoma cells. Results indicated that the effect of progesterone was not mediated through progesterone receptor. In the course of experiments, it was observed that RU-486 by itself inhibited mouse melanoma cell growth. Further research work with RU-486 showed a dose dependent inhibition of human melanoma cell growth. The mechanism of inhibition of cell growth was due to apoptosis and this effect of RU-486 was neither mediated through progesterone receptor nor glucocorticoid receptor. This in-vitro study suggested that melanoma also could be a target for RU-486 action, apart from breast, ovary and prostate cancers.