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1.
AIM To investigate the effects of long non-coding RNA (lncRNA) LINC01503 on the viability, migration and invasion of lung cancer cells and its mechanism. METHODS Human lung carcinoma H1299 cells were divided into si-NC group (transfected with si-NC), si-LINC01503 group (transfected with si-LINC01503), pcDNA group (transfected with pcDNA), pcDNA-LINC01503 group (transfected with pcDNA-LINC01503), miR-NC group (transfected with miR-NC), miR-335-5p group (transfected with miR-335-5p mimics), si-LINC01503+anti-miR-NC group (co-transfected with si-LINC01503 and anti-miR-NC), si-LINC01503+anti-miR-335-5p group (co-transfected with si-LINC01503 and anti-miR-335-5p), miR-NC+WT-LINC01503 group (co-transfected with miR-NC and WT-LINC01503), miR-NC+MUT-LINC01503 group (co-transfected with miR-NC and MUT-LINC01503), miR-335-5p+WT-LINC01503 group (co-transfected with miR-335-5p and WT-LINC01503) and miR-335-5p+MUT-LINC01503 group (co-transfected with miR-335-5p and MUT-LINC01503). The expression of miR-335-5p and LINC01503 was detected by RT-qPCR. Western blot was used to detect protein expression. MTT assay was used to detect cell viability. Transwell assay was used to detect the migration and invasion abilities. Dual-luciferase reporter assay was used to confirm the targeted relationship between LINC01503 and miR-335-5p. RESULTS Compared with normal tissues, the expression of LINC01503 was significantly increased in the lung cancer tissues, and the expression of miR-335-5p was significantly decreased (P <0.05). Compared with stage I/II , the expression level of LINC01503 in the lung cancer tissues of stage III/IV was significantly increased, and the expression of miR-335-5p was significantly decreased (P <0.05). The patients with high expression of LINC01503 had lower short-term survival rates than those with low expression of LINC01503 (P <0.05). Compared with normal human bronchial epithelial cell line BEAS-2B, the expression of miR-335-5p in lung cancer cell lines H1299, A549 and SPC-A-1 were significantly decreased, and the expression of LINC01503 was significantly increased (P <0.05). Over-expression of miR-335-5p and inhibition of LINC01503 expression inhibited the viability, migration and invasion of H1299 cells, and inhibited the protein expression of cyclin D1, matrix metalloproteinase-2 （MMP-2） and MMP-9 (P <0.05). LINC01503 targeted and regulated miR-335-5p expression, and interfering with miR-335-5p expression reversed the inhibitory effect of inhibiting LINC01503 expression on the viability, migration and invasion of H1299 cells. CONCLUSION Inhibition of lncRNA LINC01503 inhibits the viability, migration and invasion of lung cancer cells. The mechanism may be related to the targeted regulation of miR-335-5p. 相似文献
2.
AIM: To investigate the mechanism of microRNA-138-5p (miR-138-5p) inhibiting the proliferation, migration and invasion abilities of lung cancer cells.METHODS: The lung cancer A549 and H460 cells were transfected with miR-NC (control group) or miR-138-5p (experimental group). The bioinformatic analysis was performed to predict the target genes of miR-138-5p.The expression levels of miR-138-5p, forkhead box protein C1 (FOXC1) mRNA and vimentin mRNA were detected by RT-qPCR. The protein expression of FOXC1, vimentin, E-cadherin, N-cadherin and β-catenin was determined by Western blot. MTS method and colony formation assay were used to detect cell viability and proliferation ability. Wound healing assay and Transwell assay were used to detect cell migration and invasion ability.RESULTS: Over-expression of miR-138-5p significantly reduced the expression of FOXC1 and vimentin at mRNA and protein levels (P<0.05). The expression of E-cadherin and β-catenin were up-regulated and the expression of N-cadherin was down-regulated. The proliferation, migration and invasion abilities of the lung cancer cells were inhibited by the over-expression of miR-138-5p.CONCLUSION: miR-138-5p inhibits the proliferation, migration and invasion abilities of lung cancer cells by targeting FOXC1 and vimentin. It may be a potential target for lung cancer gene therapy. 相似文献
3.
LIU Hua ZHANG Su-lan LIANG Tian-song WANG Juan ZHAO Jing-yi ZHENG Ying-juan ZHANG Xiang-xian YANG Dao-ke 《园艺学报》2000,36(10):1789-1795
AIM To investigate the expression level of long noncoding RNA （lncRNA） TTN antisense RNA 1 （TTN-AS1） in lung adenocarcinoma tissues and the effects of TTN-AS1 silencing on the viability and invasion of lung adenocarcinoma A549 cells. METHODS RT-qPCR was used to detect the expression of TTN-AS1， microRNA-519d-3p （miR-519d-3p） and matrix metalloproteinase 2 （MMP2） mRNA in 32 cases of lung adenocarcinoma and adjacent normal tissues. The untransfected A549 cells were divided into blank group， si-NC group （with si-NC transfection） and si-lncRNA group （with silencing of lncRNA TTN-AS1 expression）， with n =5 in each group. The effects of TTN-AS1 silencing on the viability and invasion of A549 cells were detected by CCK8 and Transwell methods. The targeting regulatory effects of TTN-AS1 on miR-519d-3p and miR-519d-3p on MMP2 were determined by dual-luciferase reporter assay， RNA immunoprecipitation test， RT-qPCR and Western blot. RESULTS The expression level of TTN-AS1 in 32 cases of lung adenocarcinoma tissues is notably higher than that in the adjacent normal tissues （P <0.05）. Silencing of TTN-AS1 in A549 cells significantly suppressed the cell viability and invasion. TTN-AS1 negatively regulated the expression of miR-519d-3p via sponging and absorbing miR-519d-3p. MMP2 is the target gene of miR-519d-3p and can be negatively regulated by miR-519d-3p. Overexpression of MMP2 partially reversed the inhibitory effect of TTN-AS1 silencing and miR-519d-3p overexpression on the invasion of A549 cells. CONCLUSION The lncRNA TTN-AS1 is overexpressed in lung adenocarcinoma tissues， and it regulates lung adenocarcinoma A549 cell viability and invasion via miR-519d-3p/MMP2 pathway. 相似文献
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AIM: To investigate the effect of microRNA-200a (miR-200a) on the malignant biological beha-viors of breast cancer cells and its regulatory mechanism. METHODS: The expression of miR-200a in human breast can-cer cell lines MDA-MB-231, MDA-MB-468 and MCF-7, and normal human mammary epithelial cell line MCF-10A was detected by RT-qPCR. CCK-8 assay was used to detect the viability of MDA-MB-231 cells after transfection with miR-200a mimic or miR-200a inhibitor. Flow cytometry method and Transwell assay were used to detect the apoptosis and invasive ability of MDA-MB-231 cells after transfection with miR-200a mimic or miR-200a inhibitor. The expression of SIP1, E-cadherin, N-cadherin, Snail, Twist, ZEB1 and ZEB2 at mRNA and protein levels was determined by RT-qPCR and Western blot. RESULTS: Compared with MCF-10A cells, the lowest expression of miR-200a was observed in the MDA-MB-231 cells (P<0.05). Over-expression of miR-200a attenuated the viability of MDA-MB-231 cells (P<0.05), increased apoptosis (P<0.05) and decreased the invasion ability (P<0.05). The expression of SIP1, N-cadherin, Snail, Twist, ZEB1 and ZEB2 at mRNA and protein levels was also significantly down-regulated, while the mRNA and protein expression of E-cadherin was significantly increased (P<0.05). Transfection with miR-200a inhibitor reversed the above results. CONCLUSION: Up-regulation of miR-200a inhibits the viability and invasion ability of MDA-MB-231 cells and promotes the apoptosis of MDA-MB-231 cells. miR-200a may regulate the biological behaviors of breast cancer by inhibiting epithelial-mesenchymal transition. 相似文献
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AIM: To investigate the effects of microRNA-485-5p (miR-485-5p) on the viability, migration and invasion abilities of hepatocellular carcinoma cells and the underlying mechanism. METHODS: The expression levels of sex determining region Y-box 5 (SOX5) mRNA and miR-485-5p in the hepatocellular carcinoma Hep3B cells were detected by RT-qPCR with normal hepatocyte THLE-3 as control. Western blot was used to measure the expression levels of SOX5, proliferating cell nuclear antigen (PCNA), Ki67, cyclin D1 and matrix metalloproteinase-2 (MMP-2). The viability of Hep3B cells was measured by MTT assay. The migration and invasion abilities of the Hep3B cells were detected by Transwell assay. Dual-luciferase reporter assay system was applied to verify the relationship between miR-485-5p and SOX5. RESULTS: Compared with the control cells, the expression level of miR-485-5p was decreased in hepatocellular carcinoma cells Hep3B, Huh7 and HCCLM3 (P <0.05), while the expression of SOX5 at mRNA and protein levels were significantly increased (P <0.05). Over-expression of miR-485-5p inhibited the viability, migration and invasion of Hep3B cells. miR-485-5p targeted the 3′-UTR of SOX5 and negatively regulated the expression of SOX5 . Knocking-down of SOX5 expression inhibited the viability, migration and invasion of Hep3B cells. Over-expression of SOX5 partially reversed the inhibitory effect of miR-485-5p over-expression on the viability, migration and invasion of Hep3B cells. CONCLUSION: miR-485-5p inhibits the viability, migration and invasion of Hep3B cells by targeting SOX5 gene. miR-485-5p is a potential molecular target for hepatocellular carcinoma. 相似文献
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AIM:To investigate the potential mechanism of interleukin-17 (IL-17) promoting the viability, migration and invasion of human endometrial carcinoma cells. METHODS:The expression of IL-17 and microRNA-195-5p (miR-195-5p) in the human endometrial carcinoma and benign uterine lesion samples were detected by RT-qPCR. The expression of miR-195-5p in human endometrial carcinoma HEC-1-B cells after treatment with IL-17 at different concentrations for 48 h was detected by RT-qPCR. The viability, migration and invasion of HEC-1-B cells after treatment with IL-17 at 100 μg/L or transfection of miR-195-5p mimics were detected by MTT assay and Transwell assays. The viability, migration and invasion of HEC-1-B cells after over-expression of miR-195-5p combined with 100 μg/L IL-17 intervention were also observed. RESULTS:The expression of IL-17 was increased while the expression of miR-195-5p was decreased in the human endometrial carcinoma samples (P<0.05). The expression of miR-195-5p in the HEC-1-B cells after treatment with IL-17 at 10,100 and 300 μg/L for 48 h was significantly decreased (P<0.05). The results of MTT assay and Transwell experiments indicated that IL-17 at 100 μg/L enhanced the viability, migration and invasion of HEC-1-B cells, while over-expression of miR-195-5p resulted in the opposite effect. CONCLUSION:Over-expression of miR-195-5p inhibits the enhancing effects of IL-17 on the viability, invasion and migration of HEC-1-B cells. 相似文献
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CHEN Xing-feng WANG Ying-qiong CHEN Ya-hong WANG Mao-ze CHEN Shan XU Tie-feng SHI Hui-fang 《园艺学报》2019,35(9):1537-1544
AIM: To explore the function and molecular mechanism of long non-coding RNA CASC2 in non-small-cell lung cancer (NSCLC) cell migration and invasion. METHODS: RT-qPCR and Western blot were used to detect the expression of CASC2, microRNA-18a (miR-18a) and BTG3 in human bronchial epithelial cell line 16-HBE, and NSCLC cell lines A549 and H1299. The interaction between CASC2 and miR-18a or miR-18a and BTG3 was predicted by bioinformatics software and verified by double-luciferase reporter assays. Transwell assays were performed to detect the migration and invasion abilities of the NSCLC cells. RT-qPCR and Western blot were used to determine the regulatory effects of CASC2 on miR-18a and BTG3 expression. RESULTS: Compared with 16-HBE cells, the expression of CASC2 and BTG3 was significantly down-regulated in the NASCL cells, while miR-18a was significantly over-expressed (P<0.05). CASC2 acted as a molecular sponge for miR-18a, and BTG3 was verified to be a target gene of miR-18a. Up-regulation of CASC2 inhibited the migration and invasion abilities of NSCLC cells, while exogenous restoration of miR-18a stimulated cell migration and invasion abilities. In addition, exogenously over-expressed miR-181a reversed the promoting effect of CASC2 on BTG3 protein expression. CONCLUSION: CASC2 promotes BTG3 expression by negatively regulating miR-18a, and then inhibits the migration and invasion abilities of NSCLC cells. 相似文献
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AIM:To investigate the effect of microRNA-499 (miR-499) on myocardial injury in rats and its mechanism. METHODS:The rat model of ischemia-reperfusion (I/R) injury was established and the myocardial cells were primarily cultured. The expression level of miR-499 was detected by RT-qPCR. After hydrogen peroxide stimulation, CCK-8 assay and LDH kit were used to detect the viability and LDH release of the cells transfected with miR-499 mimic and siR-PTEN. The targeting relationship between miR-499 and PTEN was predicted by TargetScan and confirmed by luciferase test. RT-qPCR and Western blot were used to detect the effect of miR-499 mimic and inhibitor on the mRNA and protein expression levels of PTEN. After miR-499 inhibitor and siR-PTEN were co-transfected into the cells, CCK-8 assay and LDH kit were used to detect the viability and LDH release of the myocardial cells induced by hydrogen peroxide. RESULTS:The expression level of miR-499 in the I/R rats was increased rapidly, and then was decreased gradually in a time-dependent manner (P<0.05). miR-499 mimic and siR-PTEN significantly promoted the viability and decreased the LDH release of cardiomyocytes induced by hydrogen peroxide (P<0.05). miR-499 and PTEN had a targeting relationship. The expression of PTEN was significantly down-regulated by miR-499 mimic, and up-regulated by miR-499 inhibitor (P<0.05). Transfection with siR-PTEN reversed the inhibitory effect of miR-499 inhibitor on the cells. CONCLUSION:miR-499 attenuates the myocardial injury in rats by targeting PTEN. 相似文献
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AIM: To investigate the effects of resveratrol on the viability, invasion and autophagy of osteosarcoma MG-63 cells and the regulatory effect of microRNA-34a (miR-34a). METHODS: MG-63 cells were divided into 6 groups:control group and resveratrol treatment groups at doses of 10, 20, 40, 60 and 80 μmol/L. MTT assay, Transwell chamber method and Western blot were used to detect the effects of resveratrol on the viability, invasion ability and expression of autophagy-related proteins in the osteosarcoma cells. The effect of resveratrol at different concentrations on the expression of miR-34a in the osteosarcoma cells was detected by RT-qPCR. The effects of miR-34a mimic and miR-34a mimic negative control (miR-34a NC) transfection on the viability and invasion ability of osteosarcoma cells after treated with resveratrol at different concentrations were analyzed. The effects of miR-34a mimic transfection on autophagy-related proteins LC3-I, LC3-Ⅱ and beclin-1 were determined by Western blot. RESULTS: Compared with control group, resveratrol inhibited the viability and invasion ability of the MG-63 cells and promoted autophagy (P<0.05). Resveratrol up-regulated the expression of miR-34a in the MG-63 cells in a dose-dependent manner (P<0.05). In addition, the ratio of LC3-Ⅱ/LC3-I was increased, and beclin-1 was up-regulated (P<0.05). Co-treatment with miR-34a mimic and resveratrol increased inhibitory effects of resveratrol on the viability and invasion ability and invasion of the MG-63 cells and also promoted autophagy. CONCLUSION: Resveratrol inhibits the viability and invasion of osteosarcoma MG-63 cells and promotes auto-phagy by up-regulating miR-34a expression. 相似文献
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AIM:To investigate the underlying mechanisms of mircoRNA-497 (miR-497) inhibiting the viability, migration and invasion of papillary thyroid cancer (PTC) cells. METHODS:TargetScan 6.0 was used to predict the potential targets of miR-497. The target gene was confirmed by luciferase reporter assay, RT-qPCR and Western blot. The expression levels of miR-497 and its target gene in the PTC tissues were detected by RT-qPCR. Gene transfection, MTT assay, and cell migration and invasion assays were used to investigate the effects of miR-497 and its target gene on PTC cell viability, migration and invasion. RESULTS:AKT3 was demonstrated to be the direct target gene of miR-497. In addition, AKT3 expression was higher in the PTC tissues than that in normal tissues (P<0.05) and negatively correlated with miR-497 expression (r=-0.573 7, P<0.01). Furthermore, down-regulation of AKT3 also suppressed cell viability, migration and invasion of PTC, which played similar roles of miR-497 over-expression in PTC cells. CONCLUSION:miR-497 inhibits the viability, migration and invasion of PTC cells by directly targeting AKT3. 相似文献
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AIM: To explore the effects of microRNA-129-3p (miR-129-3p) on the viability and migration of NIH3T3 cells during transforming growth factor-β (TGF-β)-induced transformation into myofibroblasts and the underlying molecular mechanisms. METHODS: RT-qPCR was used to examine the relative expression of miR-129-3p in renal cell carcinoma (RCC)-adjacent tissues and fibrotic renal tissue. NIH3T3 cells were stimulated with TGF-β to transform into myofibroblasts, and miR-129-3p expression level was detected. After transfection with miR-129-3p mimics for 48 h in vitro, the cell viability was measured by MTT assay, the protein expression level of Ki-67 was determined by Western blot, and the cell migration was observed by wound healing assay. The direct target of miR-129-3p was predicted by online database TargetScan and confirmed by dual-luciferase reporter assay. The expression level of target protein was further confirmed by Western blot. RESULTS: Compared with the RCC-adjacent tissues, the expression of miR-129-3p was down-regulated in fibrotic renal tissue (P<0.01). In TGF-β-induced NIH3T3 cell transformation into myofibroblasts, the expression of miR-129-3p was also decreased (P<0.01). Transfection with miR-129-3p mimics followed by TGF-β stimulation in the NIH3T3 cells inhibited the viability, Ki-67 expression and migration. TargetScan analysis showed miR-129-3p had binding sites in the 3'-UTR of Smad3, which was confirmed by dual-luciferase reporter assay. The results of Western blot further confirmed that miR-129-3p affected the expression of Smad3. CONCLUSION: miR-129-3p inhibits the viability and migration ability of NIH3T3 cells during TGF-β-induced transformation into myofibroblasts by directly targeting Smad3. 相似文献
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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 . 相似文献
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AIM:To investigate the effect of microRNA-23b-3p (miR-23b-3p) on the viability and apoptosis of rheumatoid arthritis synovial fibroblasts by targeting X-linked inhibitor of apoptosis protein (XIAP). METHODS:The expression of miR-23b-3p and XIAP was detected by RT-qPCR. The TargetScan was used to predict the targeting regulatory relation between miR-23b-3p and XIAP, and then the regulatory relation was confirmed by dual-luciferase reporter assay. After the miR-23b-3p mimic and inhibitor were transfected into the cells, the expression of miR-23b-3p and XIAP was detect by RT-qPCR. The effect of miR-23b-3p on the viability and apoptosis was measured by CCK-8 assay and flow cytometry. The protein expression levels of Ki67 and Bcl-2 were determined by Western blot. RESULTS:The expression level of miR-23b-3p was down-regulated significantly (P<0.05), and XIAP was up-regulated significantly in rheumatoid arthritis synovial fibroblasts (P<0.05). The miR-23b-3p mimic significantly inhibited XIAP expression and the cell viability, promoted the apoptosis, and down-regulated the expression of Ki67 and Bcl-2 (P<0.05). The effects of miR-23b-3p inhibitor were the opposite. CONCLUSION:miR-23b-3p inhibits the viability and promotes apoptosis of rheumatoid arthritis synovial fibroblasts by targeting XIAP. 相似文献
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AIM: To investigate the effect of microRNA-486 (miR-486) on lipopolysaccharide (LPS)-induced apoptosis of alveolar epithelial cell A549. METHODS: A549 cells were treated with LPS, and the expression of miR-486 was detected by RT-qPCR. miR-486 mimics were transfected into LPS-induced A549 cells, and RT-qPCR was used to detect the up-regulation effect. The apoptotic rate was analyzed by flow cytometry and the protein levels of cleaved caspase-3 (C-caspase-3) and C-caspase-9 were determined by Western blot. The target gene prediction software was used to predict the target gene PTEN of miR-486. Luciferase reporter vector was used to identify the target relationship. pcDNA 3.1-PTEN and miR-486 mimics were co-transfected into A549 cells to detect the effect of PTEN up-regulation on apoptosis of miR-486 mimics transfected A549 cells stimulated with LPS. RESULTS: After LPS treatment, the expression of miR-486 in A549 cells was significantly decreased (P<0.05). Transfection of miR-486 mimics significantly up-regulated the expression of miR-486 in A549 cells stimulated with LPS (P<0.05). The apoptotic rate of A549 cells and the protein levels of C-caspase-3 and C-caspase-9 were significantly increased after LPS treatment (P<0.05). Up-regulation of miR-486 significantly down-regulated LPS-induced apoptosis of A549 cells (P<0.05). The expression of PTEN was negatively regulated by miR-486. Transfection of pcDNA 3.1-PTEN significantly increased the expression of PTEN, promoted the apoptosis and increased the protein levels of C-caspase-3 and C-caspase-9 in A549 cells stimulated with LPS after co-transfection with miR-486 mimics(P<0.05). CONCLUSION: miR-486 inhibits PTEN expression and reduces LPS-induced apoptosis of A549 cells. 相似文献
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AIM:To explore the effect of microRNA-125a-5p (miR-125a-5p) on cisplatin (DDP) resistance of non-small-cell lung cancer A549/DDP cells and its related mechanisms. METHODS:The expression levels of miR-125a-5p and LIM kinase 1 (LIMK1) in non-small-cell lung cancer tissues, A549 cells and A549/DDP cells were detected by RT-qPCR. The A549/DDP cell viability, apoptotic rate and expression of drug resistance-related proteins after over-expression or knockdown of miR-125a-5p and/or LIMK1 expression were detected by MTT assay, flow cytometry and Western blot, respectively. The targeting relationship between miR-125a-5p and LIMK1 was verified by TargetScan online prediction and dual-luciferase reporter system. The cell viability, apoptotic rate and expression of drug resistance-related proteins after co-expression of miR-125a-5p and LIMK1 were also determined. RESULTS:The expression level of miR-125a-5p was down-regulated and LIMK1 expression was up-regulated in non-small-cell lung cancer tissues and cell lines (P<0.05). The results of dual-luciferase assay indicated that miR-125a-5p negatively regulated the expression of LIMK1. The expression of drug resistance-related proteins and the viability of A549/DDP cells were inhibited after over-expression of miR-125a-5p or knockdown of LIMK1, while the apoptosis was enhanced. Over-expression of LIMK1 attenuated the inhibitory effect of miR-125a-5p on A549/DDP cell viability and drug resistance-related protein expression (P<0.05). CONCLUSION:miR-125a-5p reverses the resistance of A549/DDP cells to DDP by inhibiting the expression of LIMK1 and drug resistance-related proteins. 相似文献
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AIM:To explore the function and significance of microRNA-330 (miR-330) in the development of gastric cancer. METHODS:Forty-eight cases of gastric cancer tissues and paired adjacent tissues were collected in Department of Oncology, Affiliated Hospital of Gansu University of Chinese Medicine, and the expression levels of miR-330 were detected by RT-qPCR. The expression levels of miR-330 in the gastric cancer cells and human gastric epithelial GES-1 cells were evaluated by RT-qPCR. The viability, colony formation and migration of gastric cancer cells after transfected with miR-330 inhibitor or miR-330 mimic were analyzed by CCK-8 assay, colony formation assay and Transwell assay, respectively. Furthermore, miR-330 target gene was predicted by miRanda target gene prediction database. RESULTS:miR-330 expression was down-regulated both in gastric cancer tissues and gastric cancer cells (P<0.05). The expression levels of miR-330 were negatively associated with the tumor size, lymph metastasis, pathological grade stage and T stage (P<0.05). The viability, colony formation and migration of gastric cancer cells were significantly increased after transfected with miR-330 inhibitor (P<0.05). However, the viability, colony formation and migration of gastric cancer cells were significantly decreased after transfected with miR-330 mimic (P<0.05). Furthermore, EGR-2 was the direct target gene of miR-330. CONCLUSION:miR-330 suppresses gastric cancer cell growth and migration, and the mechanism may be related to its direct target gene EGR-2, suggesting that miR-330 may be used as a potential new target for diagnosis and targeted therapy for gastric cancer. 相似文献
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AIM: To investigate the regulatory effects of microRNA (miR)-195 on the biological behaviors, such as viability, apoptosis and migration, of lung cancer A549 cells, and to explore the related mechanisms. METHODS: After miR-195 mimics were transfected into the A549 cells, the cell viability, cell cycle distribution and apoptosis were measured by CCK-8 assay and flow cytometry. Transwell assay was used to detect cell migration ability. Furthermore, the protein levels of cyclin D1, CDK2, Bcl-2 and p-Rb/Rb were determined by Western blot. Dual-luciferase reporter assay was used to screen and identify the possible target genes of miR-195. RESULTS: Over-expression of miR-195 in the A549 cells inhibited the cell viability and induced cell cycle arrest, accompanied with the decrease in the cell migration ability and the increase in the apoptotic rate (P<0.05). Furthermore, the protein levels of cyclin D1, CDK2, Bcl-2 and p-Rb were significantly decreased (P<0.05). Dual-luciferase reporter assay demonstrated that MYB was a potential target gene of miR-195. Over-expression of MYB in the A549 cells partially reversed the effects of miR-195 on the cell viability, apoptosis and migration. CONCLUSION: miR-195 inhibits lung cancer A549 cell growth and migration, and promotes cell apoptosis by targeting MYB gene. 相似文献