Baicalein inhibits proliferation and migration of gastric cancer MGC-803 cells

AIM: To investigate the effects of baicalein (BAI) on the proliferation and migration of gastric cancer MGC-803 cells and the mechanisms. METHODS: After MGC-803 cells were treated with BAI at different concentrations, the viability of the MGC-803 cells was tested by MTT assay. The cell colony formation ability were detected by plate colony formation assay. Wound-healing and Transwell cell migration assays were used to test the migration ability of the MGC-803 cells. The concentration of 12-hydroxyeicosatetraenoic acid (12-HETE) was measured by ELISA. The protein levels of platelet type 12-lipoxygenase (p12-LOX), vascular endothelial growth factor (VEGF), p-ezrin and epithelial-mesenchymal transition (EMT) markers in MGC-803 cells were determined by Western blot. RESULTS: BAI significantly inhibited the proliferation, plate colony formation and migration abilities of the MGC-803 cells (P<0.05 or P<0.01), down-regulated the concentration of p12-LOX metabolite 12-HETE significantly (P<0.05 or P<0.01), decreased the protein levels of p12-LOX, VEGF, p-ezrin, vimentin and Snail (P<0.05 or P<0.01), and increased the protein expression of E-cadherin (P<0.01). CONCLUSION: BAI suppresses the proliferation and migration abilities of gastric cancer MGC-803 cells effectively. These effects of BAI may be related to regulating the protein levels of p12-LOX, VEGF, p-ezrin and EMT-related proteins.     

Promoting cell viability and migration of gastric cancer cells by PRRX2 via activation of Wnt/β-catenin signaling pathway

AIM: To study the effect of paired-related homeobox 2 (PRRX2) gene on the viability and migration ability of gastric cancer cells, and to analyze the underlying mechanism of regulating Wnt/β-catenin signaling pathway.METHODS: The expression of PRRX2 in gastric cancer and normal gastric tissue and the correlation between PRRX2 expression in gastric cancer tissues with the overall survival rate of gastric cancer patients were analyzed by bioinformatics. The small interfering RNA (siRNA) and over-expressed plasmids of PRRX2 were transfected into gastric cancer cells MGC-803 and SGC-7901, respectively. MTT assay and Transwell assay were used to detect the viability and migration ability of gastric cancer cells. Western blot and TOPflash/FOPflash dual-luciferase reporter gene assay were used to detect the activity of Wnt/β-catenin signaling pathway. Co-immunoprecipitation was used to detected the interaction between PRRX2 and β-catenin proteins.RESULTS: Knockdown of PRRX2 attenuated the viability and migration ability of gastric cancer cell line MGC-803 (P<0.05). Over-expression of PRRX2 enhanced the viability and migration ability of SGC-7901 cells (P<0.05), increased the protein levels of β-catenin, c-Myc and cyclin D1 (P<0.05) and the activity of TOPflash/FOPflash dual-luciferase reporter gene (P<0.05). PRRX2 interacted with β-catenin protein in gastric cancer cells.CONCLUSION: PRRX2 promotes the viability and migration ability of gastric cancer cells, which may be related to Wnt/β-catenin signaling pathway.     

Effect of CD97 gene silencing by small interfering RNA on migration and invasion of gastric carcinoma cell lines

AIM: To investigate the effect of CD97 gene silencing by small interfering RNA(siRNA) on migration and invasion of gastric carcinoma cell lines. METHODS: Gastric carcinoma cell lines AGS and MGC803 were used in the study. Four pairs of siRNA were designed according to the sequence of CD97 gene and synthesized chemically. The siRNAs were transfected into the gastric carcinoma cell lines. Forty-eight hours after transfection, the total RNA was extracted and the mRNA expression of CD97 was detected by real-time RT-PCR so as to screen the most effective siRNA. The protein level of CD97 was also measured by fluorescence-activated cell sorting (FACS) 72 h after Transfection. The abilities of migration and invasion were evaluated by Transwell test. The viability of the cells was measured by MTT method. RESULTS: Real-time RT-PCR and FACS revealed that CD97-siRNA notably down-regulated CD97 expression at both mRNA and protein levels. The mRNA level decreased by (89.34±9.95)% and (95.42±1.93)% in AGS and MGC803 cells,respectively. The protein levels of CD97^EGF and CD97^stalk in AGS cells decreased by (19.29±3.45)% and (30.11±5.93)%,respectively. The protein levels of CD97^EGF and CD97^stalk in MGC803 cells decreased by (26.25±5.73)% and (16.22±3.23)%,respectively. No change of the cell viability after siRNA transfection was observed. The cell number of migration and invasion in AGS cells was decreased by (67.63±12.03)% and (68.02±15.63)%,respectively. The cell number of migration and invasion in MGC803 cells was decreased by (14.92±2.03)% and (22.09±5.43)%,respectively. CONCLUSION: The siRNA effectively inhibits CD97 expression and restrains the migration and invasion capacities of gastric carcinoma cell lines, suggesting that CD97 plays an important role in the metastasis of gastric cancer.     

Effects of RARG on viability and migration ability of gastric cancer cells

AIM:To investigate the effect of retinoic acid receptor gamma (RARG) on the viability and migration ability of gastric cancer cells. METHODS:The expression of RARG in gastric cancer and normal gastric tissues and its correlation with the overall survival rate of gastric cancer patients were analyzed by bioinformatics. The expression of RARG was promoted and inhibited by over-expression plasmid transfection and RNA interference technique in gastric can-cer cells in vitro, respectively. MTT and Transwell assays were used to detect the effect of RARG on the viability and migration ability of gastric cancer cells. The effect of RARG on regulating the Wnt/β-catenin signaling pathway was evaluated by Western blot and TOP/FOP dual-luciferase reporter assay. The protein interaction of RARG and β-catenin was determined by co-immunoprecipitation and immunofluorescence co-localization assay. RESULTS:Over-expression of RARG enhanced the viability and migration ability of gastric cancer SGC7901 cells (P<0.05). Knockdown of RARG attenuated the viability and migration ability of gastric cancer MGC-803 cells (P<0.05). At the same time, RARG over-expression increased the protein expression levels of β-catenin, c-Myc, cyclin D1, Twist and Snail (P<0.05), and the activity of TOP/FOP dual-luciferase reporter gene (P<0.05). In addition, RARG interacted with β-catenin protein in the gastric cancer cells. CONCLUSION:RARG promotes the viability and migration ability of gastric cancer cells via activating the Wnt/β-catenin signaling pathway, thus playing an important role in the development of gastric cancer.     

Role of HMGA2 in epithelial-mesenchymal transition of gastric cancer cells

AIM:To investigate the role of HMGA2 in the epithelial-mesenchymal transition (EMT) in gastric cancer cells. METHODS:The expression of HMGA2 in human gastric cancer cell lines with different degrees of differen-tiation (MKN45, MKN28 and SGC7901) and immortalized human gastric epithelial cell line GES-1 was determined by Western blot and RT-qPCR. pcDNA3.0-HMGA2 plasmid was transfected into the MKN28 cells by liposome method. Transfection of si-HMGA2 interference fragments into MKN45 cells was also performed. The transfection efficiency was evaluated by Western blot and RT-qPCR. The effects of HMGA2 over-expression in the MKN28 cells and knock-down in the MKN45 cells on the cell viability were measured by CCK-8 assay. The effects of HMGA2 over-expression in the MKN28 cells on the cell migration and invasion abilities were detected by wound healing and Transwell invasion assays. The effects of HMGA2 over-expression in the MKN28 cells and knock-down in the MKN45 cells on the expression of EMT-related markers E-cadherin, N-cadherin, vimentin at mRNA and protein levels were determined by RT-qPCR and Western blot. The changes of Wnt/β-catenin signaling pathway-related molecules in the MKN28 cells with HMGA2 over-expression were also determined by RT-qPCR. RESULTS:The expression levels of HMGA2 were quite different in different differentiation levels of gastric cancer cells (P<0.05). The increased expression level of HMGA2 in MKN28 cells inhibited the cell viability (P<0.05), while the decreased expression level of HMGA2 in MKN45 cells promoted the cell viability (P<0.05). The increased expression level of HMGA2 in MKN28 cells promoted cell migration and invasion (P<0.05), changed the expression of EMT-related markers (P<0.05), while the decreased expression level of HMGA2 in the MKN45 cells changed the expression of EMT-related markers (P<0.05). The increased expression level of HMGA2 in the MKN28 cells significantly increased the mRNA levels of β-catenin in the Wnt/β-catenin pathway and the downstream molecules c-Myc and cyclin D1 (P<0.05). CONCLUSION:HMGA2 is closely related to the migration and invasion abilities of gastric cancer cells. Moreover, it promotes the EMT process of gastric cancer cells by activating Wnt/β-catenin pathway.     

miRNA-101-3p inhibits proliferation and migration of gastric cancer cells by targeting EZH2

AIM: To investigate the role of microRNA-101-3p (miRNA-101-3p) on the proliferation, apoptosis and invasion of gastric cancer cells and the possible regulatory mechanisms. METHODS: The expression of miRNA-101-3p in two kinds of gastric cancer cells and a gastric mucosal cell line was detected by real-time PCR. The miRNA-101-3p was overexpressed by Lipofectamine 2000 transfection with miRNA-101-3p mimics. The effects of miRNA-101-3p on cell cycle distribution and apoptosis were analyzed by flow cytometry. The effects of miRNA-101-3p on cell proliferation and migration abilities were detected by CCK-8 assay, trypan blue exclusion test and Transwell assay. The protein expression of enhancer of zeste homolog 2 (EZH2) was determined by Western blot. RESULTS: The expression of miRNA-101-3p in gastric cancer cells was lower than that in gastric mucosal cells (P<0.05). The gastric cancer cell MGC-803 had the lowest expression level of miRNA-101-3p. The result of flow cytometry showed that the population of S phase was reduced, and the population of G₀/G₁ phase and the early stage apoptotic rate were increased after the expression of miRNA-101-3p was overexpressed (P<0.05). The results of CCK-8 assay, trypan blue exclusion test and Transwell assay showed that overexpression of miRNA-101-3p significantly reduced the proliferation and migration abilities of gastric cancer cells (P<0.05). Overexpression of miRNA-101-3p decreased the protein level of EZH2 (P<0.05). CONCLUSION: miRNA-101-3p may suppresses the gastric cancer cell proliferation and migration, and promotes the gastric cancer cell apotosis by down-regulation of EZH2.     

High expression of BIRC5 enhances cell viability,inhibits apoptosis and is associated with poor prognosis in gastric cancer

AIM To investigate the expression of baculoviral inhibitor of apoptosis protein repeat-containing protein 5 （BIRC5） in gastric cancer tissue and its relationship with prognosis of gastric cancer patients, and to explore the effect of BIRC5 knock-down on the viability and apoptosis of gastric cancer cells. METHODS The expression of BIRC5 was detected by immunohistochemistry in 67 cases of gastric cancer tissues and paracancerous tissues for analyzing the relationships with clinicopathological characteristics. The mRNA and protein expression levels of BIRC5 in gastric carcinoma cell lines （AGS, MKN-1 and MGC-803） and normal gastric epithelial cell line GES-1 were detected by RT-qPCR and Western blot. The AGS cells were divided into blank group （no treatment）, Ctr-sh group （blank plasmid transfection） and BIRC5-sh group （BIRC5-shRNA plasmid transfection）. The interference efficiency of BIRC5-shRNA was evaluated by Western blot. The cell viability was measured by MTT assay, the apoptosis was analyzed by flow cytometry, and the levels of apoptosis-related proteins cleaved caspase-3, Bax and Bcl-2 were determined by Western blot. RESULTS BIRC5 was mainly expressed in cytoplasm, and the positive expression rate of BIRC5 in the gastric cancer tissues was higher than that in the adjacent tissues （P<0.01）. The positive rates of BIRC5 in the gastric cancer patients at TNM Ⅲ~Ⅳ stages and with lymph node metastasis were higher than those in the patients at TNM Ⅰ~Ⅱ stages and without lymph node metastasis, respectively （P<0.05）. The survival time of the patients with positive BIRC5 expression was shorter than that of the patients with negative BIRC5 expression （P=0.011 2）. The cell viability in BIRC5-sh group was lower than that in blank group and Ctr-sh group at time points of 48, 72 and 96 h. The apoptotic rate in BIRC5-sh group was increased compared with blank group and Ctr-sh group. The protein levels of cleaved caspase-3 and Bax in BIRC5-sh group were higher than those in blank group and Ctr-sh group, while the protein expression of Bcl-2 in BIRC5-sh group was lower than that in blank group and Ctr-sh group （P<0.05）. CONCLUSION High expression of BIRC5 in gastric cancer indicates poor prognosis. BIRC5 promotes the growth of gastric cancer cells and inhibits apoptosis.     

Indomethacin induces gastric cancer cell apoptosis through Akt/GSK3β/NAG-1 pathway

AIM: To investigate whether indomethacin induces gastric cancer cell apoptosis through Akt/GSK3β/NAG-1 pathway.METHODS: Gastric cancer cell line MGC-803 was used in the study. Cell viability was measured by MTT method. Hoechst 33258 nuclear staining and flow cytometry analysis were used to determine apoptosis. The protein expression level was examined by Western blotting. RESULTS: Indomethacin induced MGC-803 cell apoptosis via caspase-dependent pathway. Indomethacin inhibited Ser473-Akt and Ser9-GSK3β phosphorylation and up-regulated the expression of non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1). Inhibition of PI3K or Akt alone also increased NAG-1 expression. Moreover, the effect of indomethacin on NAG-1 expression was abolished by pretreatment of the cells with GSK3β inhibitor SB216763. CONCLUSION: Indomethacin induces gastric cancer cell apoptosis through Akt/GSK3β/NAG-1 pathway.     

Effects of NOB1 gene silencing on drug sensitivity and invasion and migration abilities of human colon cancer SW480 cells

AIM:To investigate the effect of NOB1 gene expression knock-down by transfection of small interfering RNA (siRNA) on the viability, drug sensitivity, apoptosis, cell cycle distribution, and invasion and migration abilities of human colon cancer SW480 cells. METHODS:NOB1 siRNA was transfected into SW480 cells using Lipofectamine 3000. The mRNA and protein levels of NOB1 in the SW480 cells were determined by real-time PCR and Western blot. The cell viability and sensitivity to different chemotherapeutic drugs (cisplatin, 5-fluorouracil, oxaliplatin and capecitabine) were detected by MTT assay after knock-down of NOB1 gene expression in the SW480 cells. The apoptosis and cell cycle distribution of SW480 cells were analyzed by flow cytometry. The invasion and migration abilities of SW480 cells were detected by Transwell assay. RESULTS:After transfection with NOB1 siRNA, the mRNA and protein levels of NOB1 in the SW480 cells were significantly decreased (P<0.05). Compared with control group and control siRNA group, the viability of SW480 cells in NOB1 siRNA group was significantly decreased at 24~72 h. The half maximal inhibitory concentrations of the chemotherapy drugs cisplatin, 5-fluorouracil, oxaliplatin and capecitabine were significantly decreased. The apoptotic rate was significantly increased and the cell cycle were blocked. The cell invasion and migration abilities were significantly reduced (P<0.05). CONCLUSION:Knock-down of NOB1 gene expression inhibits the viability and invasion and migration abilities of colon cancer SW480 cells, and promotes drug sensitivity and apoptosis. NOB1 may be a new target for diagnosis and treatment of colon cancer.     

Effect of oncogenic microRNA-106a on growth of normal gastric mucous epithelial cells and gastric cancer cells

AIM: To investigate the oncogenic effect of microRNA-106a (miR-106a) on normal gastric mucous epithelial cells and gastric cancer cells.METHODS: The miR-106a mimic was transfected into normal gastric mucous epithelial cell line GES-1 using liposome. The change of cell growth was measured by MTT assay. The miR-106a inhibitor was transfected into gastric cancer cell lines MGC-803 and SGC-7901 using liposome, and the changes of cell cycle distribution and cell cycle-related protein expression were measured by flow cytometry and Western blotting,respectively. The growth of gastric cancer was also observed using nude mouse xenograft model. RESULTS: The miR-106a mimic increased the growth of GES-1 cells in a dose-dependent manner. By decreasing the expression of cyclin-dependent kinase (CDK) 1 and CDK2, the miR-106a inhibitor arrested MGC-803 cells at G₀/G₁ and G₂/M phases. The miR-106a inhibitor also arrested SGC-7901 cells at G₂/M phase by decreasing the expression of CDK1. The results of animal experiments showed that the miR-106a inhibitor significantly suppressed the tumor growth in a dose-dependent manner.CONCLUSION: miR-106a may play an important role in the development of gastric cancer.     

Ursolic acid inhibits migration and invasion of human lung cancer A549 cells by targeting miRNA-133a

AIM: To investigate the effects of ursolic acid (UA) on the migration and invasion of human lung cancer cell line A549, and to explore its mechanism. METHODS: The cell viability was detected by MTT assay. The expression of miRNA-133a was detected in the A549 cells treated with UA by real-time PCR. The miRNA-133a mimics and inhibitor were transfected into the A549 cells, and the transfection efficiency was analyzed by real-time PCR. The cell migratory and invasive abilities were determined by wound healing and Transwell methods, respectively. RESULTS: The viability of the human lung cancer A549 cells was significantly inhibited by UA in a dose-dependent manner (P<0.05). IC₅₀ of UA (24 h) for lung cancer A549 cells was 31.04 μmol/L. UA treatment significantly inhibited the migratory and invasive abilities of A549 cells in a concentration-dependent manner, accompanied by significantly elevation of miRNA-133a expression. The mimics and inhibitor of miRNA-133a significantly upregulated and downregulated the expression of miRNA-133a in the transfected A549 cells, respectively. In addition, the viability of the A549 cells was decreased extremely after tansfected with the miRNA-133a mimics (P<0.01), so did the results of the cell migration and invasion test. The A549 cells tansfected with the miRNA-133a inhibitor showed an opposite changes of the cell viability, migration and invasion. CONCLUSION: UA inhibited the viability, migration and invasion of lung cancer A549 cells by elevating the expression of miRNA-133a.     

Synergistic effect of decitabine and valproic acid on apoptosis and cell cycle arrest at G0/G1 phase in gastric cancer MGC-803 cells

AIM: To investigate the synergistic effect of decitabine (DCA) and valproic acid (VPA) on apoptosis and cell cycle arrest at G₀/G₁ phase in gastric cancer MGC-803 cells. METHODS: Gastric cancer MGC-803 cells were used in the study and divided into the following groups according to the treatment with different drugs for 72 h: DCA 1.5 μmol/L,DCA 3.0 μmol/L, VPA 1.5 mmol/L, DCA 1.5 μmol/L+VPA 1.5 mmol/L and DCA 3.0 μmol/L+VPA 1.5 mmol/L. The early and late apoptotic rates were detected by annexin V and PI staining. The cell cycle was also determined by flow cytometry. The relative nm23-H1 mRNA expression level was measured by real-time quantitative PCR. RESULTS: The apoptotic rates in VPA 1.5 mmol/L+DCA 1.5 μmol/L group (early: 33.58%±3.88%; late: 31.52%±4.20%) and VPA 1.5 mmol/L+DCA 3.0 μmol/L group (early: 42.61%±4.23%; late: 38.01%±3.86%), the percentages of the cells in G₀/G₁ phase in VPA 1.5 mmol/L+DCA 1.5 μmol/L group (61.55%±2.38%) and VPA 1.5 mmol/L+DCA 3.0 μmol/L group (66.75%±2.48%), and the relative nm23-H1 mRNA expression levels in VPA 1.5 mmol/L +DCA 1.5 μmol/L group (1.84±0.46) and VPA 1.5 mmol/L+DCA 3.0 μmol/L group (3.02±0.36) were all significantly higher than those in the corresponding concentrations of single drug treatment groups (P<0.01). CONCLUSION: Synergistic effect of VPA and DCA on apoptosis and cell cycle arrest in gastric cancer MGC-803 cells is possibly via inactivation of nm23-H1 gene expression.     

Effect of IQGAP1 siRNA on biological characteristics of glioma cells by regulating STAT3 signaling pathway

AIM: To investigate the effect of IQGAP1 gene expression knock-down on invasion, migration and immunosuppression of glioma cells and its mechanism. METHODS: Human glioma U251 cells were randomly divided into blank group, negative control group and si-IQGAP1 group. AG490, an inhibitor of STAT3 signaling pathway, was used to treat the cells for 48 h. The cell viability was measured by MTT assay. The protein levels of IQGAP1, vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1), STAT3 and p-STAT3 were determined by Western blot. The cell invasion and migration abilities were detected by Transwell assays. RESULTS: The protein expression of IQGAP1 in si-IQGAP1-1 group and si-IQGAP1-2 group was significantly lower than that in blank group (P<0.05). Compared with blank group, the viability, the invasion ability and the migration ability of the cells in si-IQGAP1 group and AG490 group were significantly decreased, while the protein levels of VEGF, TGF-β1 and p-STAT3 were significantly decreased (P<0.05). Compared with AG490 group, the cell viability, invasion ability and migration ability in AG490+si-IQGAP1 group were significantly decreased, and the protein levels of VEGF and TGF-β1 were significantly decreased (P<0.05). CONCLUSION: Silencing of IQGAP1 gene expression reduces the invasion and migration abilities of glioma cells and decreases the protein expression of cellular immunosuppression molecules VEGF and TGF-β1, which is related to down-regulation of STAT3 signaling pathway.     

Celecoxib induces apoptosis in COX-2 non-expression gastric cancer cells

AIM: To investigate whether celecoxib induces gastric cancer cell apoptosis in a COX-2 non-expression cell line. METHODS: The COX-2 protein was examined by western blotting. Fluorescence microscopy, DNA agarose gel electrophoresis and flow cytometry analysis were used to test apoptosis. RESULTS: COX-2 was expressed in AGS but not MGC-803 gastric cancer cell line; Selective COX-2 inhibitor celecoxib induced MGC-803 cell line apoptosis in a concentration and time-dependent manner. CONCLUSION: Celecoxib induces apoptosis in COX-2 non-expression gastric cancer cells.     

miR-556-3p regulates viability,migration and invasion of endometrial cancer cells by targeting SASH1

AIM To investigate whether microRNA-556-3p （miR-556-3p） regulates the viability, migration and invasion of endometrial cancer cells by targeting SASH1 gene. METHODS The expression of miR-556-3p, and the mRNA and protein levels of SASH1 in endometrial cancer tissues were detected by RT-qPCR and Western blot. Anti-miR-556-3p or pcDNA-SASH1 was transfected into endometrial cancer Ishikawa cells. The cell viability was detected by MTT assay, the migration and invasion abilities of the cells were detected by Transwell chamber method, and the protein expression levels of cyclin D1, p21, matrix metalloproteinase-2 （MMP-2） and MMP-9 were detected by Western blot. StarBase prediction and dual-luciferase reporter experiments were used to analyze the targeting relationship between miR-556-3p and SASH1. Anti-miR-556-3p and si-SASH1 were co-transfected into the Ishikawa cells, and their effects on cell viability, migration and invasion were examined by the methods described above. RESULTS Compared with adjacent tissues, the expression of miR-556-3p in endometrial cancer tissues was increased significantly, and the expression of SASH1 at mRNA and protein levels was decreased significantly （P<0.05）. Inhibition of miR-556-3p expression or induction of SASH1 over-expression obviously reduced the viability of Ishikawa cells, the number of migratory cells, the number of invasive cells and the protein levels of cyclin D1, MMP-2 and MMP-9, and dramatically increased the protein level of p21 （P<0.05）. miR-556-3p targeted SASH1 and negatively regulated its expression. Knock-down of SASH1 expression reversed the inhibitory effect of miR-556-3p expression inhibition on the viability, migration and invasion of Ishikawa cells. CONCLUSION Inhibition of miR-556-3p expression suppresses the viability, migration and invasion of endometrial cancer cells. The mechanism is related to the regulation of its target gene SASH1.     

Photoactivation promotes curcumin to induce apoptosis of human gastric cancer MGC-803 cells

AIM: To investigate the effect of photoactivated curcumin on apoptosis of human gastric cancer MGC-803 cells. METHODS: The effect of photoactivated curcumin on the growth inhibitory rate of gastric cancer MGC-803 cells was detected by MTT assay. The changes of nuclear morphology were observed under optical microscope with Hoechst 33258 fluorescent staining. The apoptotic rate, mitochondrial membrane potential, intracellular reactive oxygen species and Ca²⁺ level was determined by flow cytometry. The activity of caspase-3, caspase-8 and caspase-9 was detected by colorimetry. The protein levels of cytochrome C, Bcl-2, Bax and heat-shock protein 70 (HSP70) were analyzed by Western blotting. RESULTS: The growth inhibitory rate of MGC-803 cells treated with curcumin at concentration of 5.0 μmol/L was (29.74±2.30)%.Some apoptotic cells were observed under optical microscope, and the apoptotic rate was (12.54±1.75)%. The growth inhibitory rate of MGC-803 cells treated with photoactivated curcumin was (44.93±3.61)%.Significant morphological changes in the nucleus, such as chromatin condensation and apoptotic body formation, were observed under light microscope, and the apoptotic rate was (26.58±2.67)%. The cell cycle was arrested at G₀/G₁ phase. Compared with curcumin group, significant reduction in mitochondrial membrane potential,significant increase in cytochrome C, intracellular reactive oxygen species, Ca²⁺ level and the activity of caspase-3, caspase-8 and caspase-9 were observed in photoactivated curcumin group (P<0.01). Photoactivated curcumin also significantly inhibited the protein expression of Bcl-2 and HSP70 in the cells. CONCLUSION: Photoactivated curcumin enhances the apoptosis of gastric cancer MGC-803 cells by inhibiting Bcl-2 expression and promoting the mitochondrial pathway.     

Expression of miRNA-22 in ovarian cancer and effect of miRNA-22 over-expression on SKOV-3 ovarian cancer cell proliferation,migration and invasion

AIM: To examine the expression of miRNA-22 in the ovarian tissues and the effect of miRNA-22 over-expression on the proliferation, migration and invasion in SKOV-3 cells. METHODS: The expression levels of miRNA-22 in different ovarian tissues and SKOV-3 cells were determined by qPCR. miRNA-22 was over-expressed by transfection of miRNA-22 mimic. The cell viability was examined by CCK-8 assay. The cell migration was measured by wound healing test. The cell invasion was analyzed by Transwell assay. The protein expression levels of VEGF and P53 were determined by Western blot. RESULTS: Compared with the normal ovarian tissue, the expression level of miRNA-22 was remarkably decreased in the ovarian tumor tissues. After transfection with miRNA-22 mimic, the expression level of miRNA-22 in the SKOV-3 cells was significantly increased, while the cell viability, migration and invasion were obviously decreased. Moreover, the protein expression of VEGF and P53 was dramatically inhibited after over-expression of miRNA-22. CONCLUSION: The decreased miRNA-22 expression may be correlated with the development of ovarian can-cer. Over-expression of miRNA-22 decreases the cell viability, migration and invasion by reducing the protein expression of VEGF and P53.