共查询到20条相似文献，搜索用时 46 毫秒
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AIM: To investigate the effect of Linc00152 on the viability, apoptosis and radiosensitivity of cervical cancer cells. METHODS: RT-qPCR was used to detect the expression levels of Linc00152 and microRNA-376c-3p(miR-376c-3p) in human cervical cancer HeLa cells and SiHa cells, and normal cervical Ect1/E6E7 cells. The cervical cancer HeLa cells with low Linc00152 expression or miR-376c-3p over-expression were established. MTT assay, flow cytometry, colony formation assay and Western blot were used to determine the cell viability, apoptosis, radiosensitivity and related protein expression. The dual-luciferase reporter assay was used to verify the regulatory relationship between Linc00152 and miR-376c-3p in the HeLa cells. RESULTS: Compared with the Ect1/E6E7 cells, Linc00152 was up-regulated in the HeLa cells and SiHa cells, and miR-376c-3p was down-regulated (P < 0.05). Low expression of Linc00152 or over-expression of miR-376c-3p inhibited the viability of HeLa cells, induced apoptosis, enhanced the radiosensitivity, inhibited the protein expression of cyclin D and Bcl-2, and promoted the protein expression of P21 and Bax (P < 0.05). Linc00152 negatively regulated miR-376c-3p expression in the HeLa cells, and inhibition of miR-376c-3p expression reversed the effect of low expression of Linc00152 on HeLa cell viability, apoptosis and radiosensitivity. CONCLUSION: Linc00152 is highly expressed in the cervical cancer cells. Linc00152 affects the viability, apoptosis and radiosensitivity of HeLa cells by targeting miR-376c-3p, which is a potential diagnosis and treatment target for cervical cancer. 相似文献
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AIM:To detect the serum level of miR-155-5p in the patients with different cervical diseases, and to analyze its effects on the proliferation, cell cycle and apoptosis of cervical cancer cells. METHODS:SYBR Green I real-time quantitative PCR was used to detect the level of miR-155-5p in the serum of the patients with different cervical diseases. miR-155-5p mimic or inhibitor was used to increase or decrease the expression of miR-155-5p in cervical cancer cells. The proliferation, cell cycle and apoptosis were measured by CCK-8 assay and flow cytometry. RESULTS:The serum level of miR-155-5p in cervical cancer group was higher than that in cervicitis group and healthy group. No statistical difference of the serum miR-155-5p level between cervical intraepithelial neoplasia group and cervical cancer group was observed. Compared with blank group, liposome group and negative control group, the proportion of S-phase cells increased and apoptotic cells decreased in SiHa cells transfected with 100 nmol/L and 200 nmol/L miR-155-5p mimic. The proportion of G2/M-phase cells increased significantly in SiHa cells transfected with 100 nmol/L and 200 nmol/L miR-155-5p inhibitor. CONCLUSION: Compared with healthy controls, the serum level of miR-155-5p in the cervical cancer patients increases, and may act as a novel tumor molecular marker for diagnosis of cervical cancer. miR-155-5p has no significant effect on the proliferation, cell cycle and apoptosis of HeLa cell. miR-155-5p may promote SiHa cells to enter S phase and inhibit the apoptosis of SiHa cells. 相似文献
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AIM:To investigate the molecule mechanism of microRNA (miR)-30c over-expression inhibiting malignant phenotypes of cervical cancer cells. METHODS:Cervical cancer cell lines C33A, HeLa, SiHa and CaSki were transfected with pGenesil-1-miR-30c plasmid using Lipofectamine 2000 kit, and the expression of miR-30c was determined by TaqMan real-time PCR. The cell viability inhibition rate, colony formation ability, migration rate and apoptotic rate were measured by MTT assay, colony formation assay, Transwell experiment, and flow cytometry with Annexin V-FITC staining. The protein expression of Bax, Bcl-2, matrix metalloproteinase (MMP)-9, MMP-13 and tissue inhibitor of metalloprotei-nase-1 (TIMP-1) was detected by Western blot. RESULTS:The expression levels of miRNA-30c in the cervical cancer cell lines transfected with pGenesil-1-miR-30c plasmid were significantly higher than those in negative control groups (cell lines transfected with pGenesil-1 plasmid) (P<0.01). Significantly increased cell viability inhibition rate, and decreased colony formation ability and migration rate were found in the cervical cancer cell lines over-expressing miR-30c as compared with negative control groups (P<0.05). The apoptotic rate in the cervical cancer cell lines over-expressing miR-30c was dramatically higher than that in control groups (P<0.05). Over-expression of miR-30c in cervical cancer cells promoted the protein expression of Bax and TIMP-1, and decreased the protein expression of Bcl-2 and MMP-13 (P<0.05 or P<0.01). CONCLUSION:Over-expression of miR-30c significantly inhibits the viability and migration, and induces apoptosis of cervical cancer cells. The mechanism may be related to activating apoptosis pathway and inhibiting MMP-13 protein expression. 相似文献
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TIAN Xiao-gang ZHAO Lin ZHANG Chun-lin REN Jin-xia ZHAO Feng-ju YANG Wen-cui GOU Cai-xia 《园艺学报》2018,34(8):1461-1467
AIM: To investigate the molecular biological mechanisms by which microRNA-126 (miR-126) enhances the radiosensitivity of gastric cancer cells. METHODS: SGC-7901 cells were cultured in vitro. In order to over-express miR-126 in SGC-7901 cells, miR-126 mimic was transfected. The mRNA and protein levels of enhancer of zeste ho-molog 2 (EZH2) were detected by RT-qPCR and Western blot, respectively. The targeting relationship between miR-126 and EZH2 was determined by dual-luciferase reporter assay. To estimate the effect of EZH2 on miR-126-enhanced radiosensitivity of the SGC-7901 cells, the pcDNA3.1-EZH2 vector was also co-transfected with miR-126 mimic, and then CCK-8 assay and flow cytometry were used to detect the viability and apoptotic rate of the cells after radiation. RESULTS: Over-expression of miR-126 significantly inhibited the expression of EZH2 in SGC-7901 cells both at protein and mRNA levels (P<0.05). A direct targeting relationship between miR-126 and EZH2 was confirmed by dual-luciferase reporter assay. Compared with the cells only transfected with miR-126 mimic, co-transfection of pcDNA3.1-EZH2 with miR-126 mimic increased the viability but reduced the apoptosis of the cells treated by radiation (P<0.05). CONCLUSION: Targeting inhibition of EZH2 may be one of the mechanisms by which miR-126 enhances the radiosensitivity of gastric cancer cells. 相似文献
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AIM: To explore the effect of microRNA-146a (miR-146a) on apoptosis of human gastric cancer SGC-7901 cells and the underluing mechanism. METHODS: miR-146a mimic (up-regulated miR-146a expression) and miR-146a inhibitor (down-regulated miR-146a expression) were transfected into the SGC-7901 cells by liposome method. At the same time, miRNA nonsense sequence transfection group as the negative control group (NC group) was set up. RT-qPCR was used to evaluate the levels of miR-146a in the SGC-7901 cells after transfection. The effects of miR-146a on the cell apoptosis and growth were assessed by flow cytometry analysis and CCK-8 assay, respectively. The effect of over-expression or knockdown of miR-146a on transforming growth factor-β-activated kinase 1 (TAK1)/nuclear factor-kappa B (NF-κB) signaling was evaluated by RT-qPCR and Western blot. RESULTS: miR-146a modulated apoptosis of SGC-7901 cells. Over-expression of miR-146a significantly increased apoptosis, whereas knockdown of miR-146a inhibited the apoptosis of SGC-7901 cells. The expression of TAK1 at mRNA and protein levels was significantly decreased when miR-146a mimic was transfected into the SGC-7901 cells (P<0.05). On the contrast, the expression of TAK1 at mRNA and protein were significantly higher in miR-146a inhibitor transfection group than that in NC group (P<0.05), suggesting that miR-146a negatively regulated TAK1 expression. Moreover, knockdown of TAK1 enhanced the apoptosis of SGC-7901 cells (P<0.01), while over-expression of TAK1 inhibited the apoptosis of SGC-7901 cells(P<0.01). Additionally, both over-expression of miR-146a and knockdown of TAK1 led to a prominent increase in the expression of NF-κB inhibitor protein alpha (IκBα) and a significat decrease in B cell lymphoma-2 (Bcl-2) level in the SGC-7901 cells. CONCLUSION: miR-146a significantly promotes apoptosis of SGC-7901 cells by inhibition of NF-κB pathway via targeting TAK1. 相似文献
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AIM: To investigate the inhibitory effect of microRNA-145 (miR-145) on epithelial-mesenchymal transition (EMT) in renal cancer A-498 cells. METHODS: The A-498 cells were transfected with miR-145 mimics (M145) and mimic negative control(MNC), which served as M145 group and MNC group, respectively. Mock control (MC) group was set up using untreated A-498 cells. The expression level of miR-145 in each group was detected by RT-qPCR. Transwell assay was used to detect the invasion ability of the cells. The protein expression of vimentin, E-cadherin and ADAM28 was determined by Western blot. Bioinformatic method was used to predict the target genes of miR-145. Antagonistic effect of ADAM28 over-expression on the inhibition of EMT by miR-145 was detected by Western blot. The relationship between miR-145 and ADAM28 was analyzed by dual-luciferase reporter assay. RESULTS: The expression level of miR-145 in M145 group was significantly up-regulated than that in MC group (P<0.05). The number of invasive cells in M145 group was 12.78±3.37, which was significantly lower than that in MC group (P<0.05). ADAM28 may be the target gene of miR-145. Compared with MC group, the protein expression of vimentin and ADAM28 in M145 group was significantly decreased (P<0.05), while the protein expression of E-cadherin was significantly increased (P<0.05).After ADAM28 over-expression, the protein expression of vimentin in the A-498 cells of M145 group was significantly increased (P<0.05), and the protein expression of E-cadherin was significantly decreased (P<0.05). The results of dual-lucife-irasei reporter assay showed that ADAM28 was a downstream target gene of miR-145. CONCLUSION: miR-145 may inhibit the expression of EMT-related proteins through the downstream target gene ADAM28 and inhibit the EMT process of renal cancer A-498 cells. 相似文献
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AIM:To investigate the inhibitory effect of microRNA-9(miR-9) on epithelial-mesenchymal transition (EMT) in the gastric cancer SGC-7901 cells and its mechanism.METHODS:The gastric cancer cell line SGC-7901 was transfected with miR-9 mimics or negative control mimic (NCM),as miR-9 or NCM group,respectively.The SGC-7901 cells without transfection were used as control group.The expression level of miR-9 in each group was detected by RT-qPCR.The migration and invasion abilities of the SGC-7901 cells in the 3 groups were detected by Transwell assay.The protein expression of N-cadherin,E-cadherin,α-catenin and neuropilin-1(NRP1) was determined by Western blot.Antagonistic effect of NRP1 over-expression on miR-9 inhibition of EMT was detected by Western blot.The relationship between miR-9 and NRP1 was analyzed by dual luciferase assay.RESULTS:The expression level of miR-9 in miR-9 group was significantly up-regulated,which was 538 times higher than that in control group (P<0.05).The number of migratory cells in miR-9 group was significantly lower than that in control group (P<0.05).Compared with control group,the protein expression of N-cadherin and NRP1 in miR-9 group was significantly decreased,while the protein expression of E-cadherin and α-catenin protein was significantly increased.Over-expression of NRP1 resulted in the increase in the protein expression of N-cadherin in the gastric cancer cells of miR-9 group,and the decrease in the protein expression of E-cadherin and α-catenin significantly.The result of dual luciferase assay showed that NRP1 was a downstream target gene of miR-9(P<0.05).CONCLUSION:miR-9 may inhibit the expression of EMT-related proteins through the downstream target gene NRP1,thus inhibiting the EMT of gastric cancer SGC-7901 cells. 相似文献
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YAN Cheng-quan CAI Sheng-yong MENG Bin WANG Peng-fei LI Lin ZHAO Chao-fei LIU Yi-fei MENG Xin 《园艺学报》2018,34(7):1256-1263
AIM:To investigate the biological functions of microRNA-29a (miR-29a) in prostate cancer and the molecular mechanism of miR-29a over-expression inhibiting malignant phenotypes of prostate cancer cells. METHODS:The levels of miR-29a expression in the prostate cancer tissues and cells were detected and analyzed using gene microarray and bioinformatics. The expression levels of miR-29a and lysine (K)-specific demethylase 4B (KDM4B) mRNA in prostate cancer tissues, paracarcinomatous tissues, 4 prostate cancer cell lines (PC3, DU145, LNCaP and ArCaP) and normal prostate epithelial cell line (RWPE-1) were measured by real-time PCR. PC3, DU145, LNCaP and ArCaP cells were transfected with pGenesil-1-miR-29a plasmid using transient transfection. The cell viability, colony formation rate and apoptotic rate were analyzed by MTT assay, colony formation assay and flow cytometry with Annexin V-FITC/PI staining, respectively. The protein expression of KDM4B was determined by Western blot. RESULTS:The results of gene microarray and bioinformatic analysis indicated that differential expression of miR-29a was found in the prostate cancer tissues and the paracarcinomatous tissues. The levels of miR-29a in the prostate cancer tissues and prostate cancer cells were significantly decreased, while the mRNA levels of KDM4B were notably increased compared with the paracarcinomatous tissues and RWPE-1 cells, respectively (P<0.05). Compared with negative control (pGenesil-1) group, the cell viability and colony formation rate were significantly decreased, the apoptotic rate was significantly increased, and the protein expression of KDM4B was notably inhibited in the prostate cancer cells with miR-29a over-expression (P<0.05). The cell viability was significantly enhanced, and the apoptosis was significantly inhibited in the prostate cancer cells with KDM4B over-expression (P<0.05). CONCLUSION:Low expression of miR-29a was found in the prostate cancer tissues and cells. miR-29a over-expression inhibits the growth of prostate cancer cells and induces apoptosis. The mechanism may be associated with inhibiting the protein expression of KDM4B. 相似文献
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AIM: To study the target relationship between microRNA-98 (miR-98) and enhancer of Zeste homolog 2 (EZH2), and the effect of miR-98 on the viability and invasion ability of colorectal cancer cells.METHODS: The target relationship between EZH2 and miR-98 was predicted by TargetScan software and confirmed by dual-luciferase reporter assay. The miR-98 mimic and miR-98 inhibitor were transfected into human colorectal cancer SW480 cells and SW620 cells. The protein expression level of EZH2 was determined by Western blot. The cell viability was measured by MTT assay, and the invasion ability was detected by Transwell assay. EZH2 over-expression vector was transfected into the colorectal cancer cells, and the cell viability and invasion ability were measured.RESULTS: miR-98 targeted EZH2 and down-regulated EZH2 protein expression in the SW480 cells and SW620 cells. miR-98 over-expression significantly decreased, while miR-98 knockdown dramatically increased the viability and invasion ability of SW480 cells and SW620 cells. Additionally, EZH2 over-expression enhanced the viability and invasion ability of SW480 cells and SW620 cells.CONCLUSION: miR-98 inhibits the viability and invasion ability of SW480 cells and SW620 cells by targeting EZH2, which may provide new therapeutic target and method for colorectal cancer treatment. 相似文献
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AIM:To explore the effect of microRNA-155(miR-155)over-expression on the expression of inflammatory factors and indolamine 2, 3- dioxygenase (IDO) in the microglial BV-2 cells. METHODS:For over-expression of miR-155, the BV-2 cells were transfected with lentiviral vector carrying mmu-miR-155. The expression of inflammatory factors was detected by cytometric bead array system (CBA). The mRNA expression of inflammatory factors and IDO was analyzed by real-time PCR. The protein levels of suppressor of cytokine signalling 1 (SOCS1), p-p38 MAPK and IDO were determined by Western blot. RESULTS:The expression of miR-155 was up-regulated in the BV-2 cells transfected with lentiviral vector carrying mmu-miR-155 compared with LPS treatment group (P<0.01). The miR-155 over-expression promoted the secretion of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1) and IL-10, and inhibited the secretion of IL-12. The miR-155 over-expression increased the mRNA expression of IL-6, TNF-α, IL-10 and IDO, also increased the protein levels of IDO and p-p38 MAPK, but decreased the protein expression of SOCS1 (P<0.01). LPS promoted the secretion of IL-6, TNF-α, MCP-1 and IL-12, also increased the mRNA expression of IL-6, TNF-α and IDO, meanwhile, increased the protein levels of IDO, p-p38 MAPK and SOCS1 (P<0.01). CONCLUSION:Over-expression of miR-155 promotes the secretion of related imflammatory factors and protein expression of IDO in microglial BV-2 cells mediated with SOCS1 and p38 MAPK signaling pathway. 相似文献
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AIM: To investigate the effect of miR-496 over-expression on the growth and metastasis of colon cancer cells and its molecular mechanism.METHODS: The proteins interacting with miR-496 were screened by bioinformatic method. The levels of miR-496, CTNNB1 mRNA and β-catenin protein in colon cancer cell lines, HT29, HCT116 and SW480, and normal colonic epithelial cell line NCM460 were detected by real-time PCR and Western blot. HT29, HCT116 and SW480 cells were transfected with miR-496 mimics using Lipofectamine 2000 and named as HT29-miR-496 mimics, HCT116-miR-496 mimics and SW480-miR-496 mimics cells, respectively, and the cells transfected with the scramble served as negative control. The cell viability, lactate dehydrogenase (LDH) leakage, and colony formation and metastatic abilities were determined by MTT assay, LDH assay, colony formation assay and Transwell method, respectively. The promoter activity of miR-496 was measured using luciferase reporter gene assay. The protein levels of β-catenin, eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1), p-4E-BP1, low-density lipoprotein receptor-related protein 6(LRP6), p-LRP6, MMP-7, MMP-9, MMP-13 and TIMP-2 were monitored by Western blot.RESULTS: Endogenous miR-406 interacted with β-catenin was found in the colon cancer cells. Low miR-496 expression in the HT29, HCT116 and SW480 cells and high miR-496 expression in NCM460 cells were detected. In contrast, high β-catenin expression was found in the HT29, HCT116 and SW480 cells and low β-catenin expression was observed in the NCM460 cells. Compared with control group, the cell viability, colony formation rate and the number of metastatic cells remarkably decreased in the HT29-miR-496 mimics, HCT116-miR-496 mimics and SW480-miR-496 mimic cells (P<0.05). The promoter activity of miR-496 was significantly increased in colon cancer cells transfected with miR-496 mimics, and was 1.75, 2.04 and 1.61 times as high as control group. miR-496 over-expression inhibited β-catenin levels, and p-4E-BP1 and p-LRP6 protein levels were also reduced. siRNA- or over-expressed miR-496-mediated β-catenin down-regulation inhibited MMP-7 and MMP-9 expression, but promoted TIMP-2 expression.CONCLUSION: The expression level of miR-496 in the colon cancer cells is low, but in the normal colonic epithelial cells is high. miR-496 over-expression inhibits the protein levels of MMP-7 and MMP-9, and promotes the protein expression of TIMP-2 via inhibiting Wnt/β-catenin pathway, thus suppressing malignant phenotype in the colon cancer cells. 相似文献
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AIM: To investigate the clinical significance of microRNA-326 (miRNA-326) expression in gastric carcinoma and the effect of up-regulation of its expression on the viability and apoptosis of gastric cancer cells. METHODS: The expression of miRNA-326 in 55 tissue samples of gastric cancer was detected by RT-qPCR, and the relationship between the expression and the clinicopathological features was analyzed. The expression of miRNA-326 in gastric cancer BGC-823 cells was detected by RT-qPCR. The BGC-823 cells were transfected by liposome method, and randomly divided into normal control group (untransfected), mimic-NC group (transfected with negative control mimic) and miRNA-326 mimic group (transfected with miRNA-326 mimic). After up-regulation of miRNA-326 expression, the cell viability was measured by CCK-8 assay, and the apoptosis of the cells was analyzed by flow cytometry. The protein levels of matrix metalloprotein 9 (MMP-9), p21, cyclin D1, Bcl-2 and cleaved caspase-3 were determined by Western blot, and the mRNA expression of cyclin D1 was detected by RT-qPCR. Whether CCND1 (the gene of cyclin D1) was the target gene of miRNA-326 was evaluated by dual-luciferase reporter assay. RESULTS: The expression of miRNA-326 in the gastric cancer tissues was significantly lower than that in the adjacent tissues (P<0.05). The miRNA-326 expression had a significant correlation with the tumor size, lymph node metastasis, differentiation, and clinical stages (P<0.05), but it had no correlation with the age and sex of the patients. Moreover, the expression of miRNA-326 was also closely related to the survival rate of the patients (P<0.05). The expression of miRNA-326 in the BGC-823 cells was significantly lower than that in the normal gastric mucosa GES-1 cells (P<0.05). Compared with normal control group, the expression of miRNA-326 in mimic-NC group did not change significantly, while that in miRNA-326 mimic group was increased significantly (P<0.05). Compared with normal control group, the cell viability in miRNA-326 mimic group was significantly decreased, and the apoptosis was increased (P<0.05). In addition, compared with normal control group, the protein levels of MMP-9, cyclin D1 and Bcl-2, and the mRNA expression of cyclin D1 in miRNA-326 mimic group were decreased, while the protein levels of p21 and cleaved caspase-3 were increased (P<0.05). However, no significant difference of above protein and mRNA levels between mimic-NC group and normal control group was observed. Compared with mimic-NC+miR-326 mimic group, the activity of luciferase in the cells transfected with pmiR-CCND1-WT plasmid was significantly decreased (P<0.05), but that in the cells transfected with pmiR-CCND1-Mut plasmid did not change significantly. CONCLUSION: The expression level of miRNA-326 in gastric cancer tissues is low, and it may promote cell viability and inhibit cell apoptosis by targeting CCND1. 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 clinical significance of stathmin 1 (STMN1) expression in cervical cancer and the influence of its expression on the viability and apoptosis of cervical cancer cells. METHODS: Western blot was used to detect the protein expression of STMN1 in cervical cancer tissues, and the relationship between the expression and clinical characteristics of cervical cancer was analyzed. STMN1-siRNA was transfected into cervical squamous-cell carcinoma SiHa cells. The protein levels of STMN1, STAT3, p-STAT3 and survivin were determined by Western blot after transfection for 48 h. The cell viability was measured by MTT assay. The apoptosis was analyzed by flow cytometry. DCFH-DA probe was used to detect the level of reactive oxygen species (ROS). RESULTS: The protein expression of STMN1 in cervical cancer tissues was significantly higher than that in paracancerous tissues (P<0.01). The STMN1 protein expression level was not correlated with age and histological types of cervical cancer patients, but was related to clinical stage, histological differentiation and lymph node metastasis (P<0.01). Transfection with STMN1-siRNA significantly reduced the expression of STMN1 in SiHa cells. Compared with control group, the cell viability in STMN1-siRNA group was significantly decreased, the apoptotic rate and ROS content were increased, and the protein levels of p-STAT3 and survivin were down-regulated (P<0.01). However, no significant difference of the STAT3 protein level was observed between STMN1-siRNA group and control group. CONCLUSION: STMN1 is highly expressed in cervical cancer, and its expression is related to clinical stage, histological differentiation and lymph node metastasis. Inhibition of STMN1 expression reduces the viability and promotes apoptosis of cancer cells by down-regulating STAT3 signaling pathway. 相似文献
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AIM: To explore the effect of microRNA-221 (miR-221) on the proliferation of lung cancer A549 cells, and to investigate its mechanism. METHODS: The A549 cells were transfected with miR-221 mimics by Lipofectamine 2000. The expression of miR-221 was detected by RT-qPCR. The expression of PTEN at mRNA and protein le-vels was detected by RT-qPCR and Western blot, respectively. The cell proliferation was examined by CCK-8 assay and colony formation assay. The 3'-UTR of PTEN was cloned into luciferase reporter vector and its enzymatic activity was detected to verify whether miR-221 targeted to PTEN. RESULTS: The expression level of miR-221 in the A549 cells was significantly increased after transfection with miR-221 mimics as compared with negative control group and blank group (P<0.01). The mRNA and protein levels of PTEN were significantly down-regulated compared with control group and blank group (P<0.05). In addition, miR-221 over-expression significantly promoted the proliferation of A549 cells (P<0.05). Moreover, miR-221 inhibited the enzymatic activity of luciferase reporter vector of PTEN. CONCLUSION: Over-expression of miR-221 significantly promotes the proliferation ability of human lung cancer A549 cells by down-regulation of PTEN. 相似文献
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AIM: To explore the effect of microRNA-221 (miR-221) on resistance of lung cancer cells to gefitinib, and to investigate its related mechanism. METHODS: RT-qPCR was used to detect the levels of miR-221 expression between gefitinib-sensitive cell line PC9 and gefitinib-resistant cell line PC9/GR. The PC9/GR cells were transfected with miR-221 inhibitor by Lipofectamine 2000. The drug sensitivity of these cells to gefitinib was determined by CCK-8 assay. The protein expression level of phosphatase and tensin homologue deleted on chromosome ten (PTEN) was determined by Western blot. The 3'-UTR of PTEN was cloned into luciferase reporter vector and its luciferase activity was detected to verify whether miR-221 targets PTEN. RESULTS: The expression level of miR-221 in the PC9/GR cells was significantly higher than that in the PC9 cells (P<0.05). The protein expression level of PTEN in the PC9/GR cells was lower than that in the PC9 cells (P<0.05). The IC50 of gefitinib was significantly reduced in the PC9/GR cells after transfection with miR-221 inhibitor (P<0.05). The protein expression level of PTEN in the cells transfected with miR-221 inhibitor was increased as compared with control group and blank group (P<0.05). Inhibition of miR-221 expression enhanced the enzymatic activity of luciferase reporter vector of PTEN. CONCLUSION: miR-221 enhances the resistance of lung cancer cells to gefitinib by down-regulating the protein expression of PTEN. 相似文献
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AIM: To investigate the regulatory mechanisms of microRNA-29a (miR-29a) on the expression of Bcl-2 and Mcl-1 in rat cardiomyocytes (CM cells). METHODS: The CM cells were isolated from the hearts of newborn rats and transfected with miR-29a mimic (100 nmol/L) by Lipofectamine RNAiMAX. The expression of Bcl-2 and Mcl-1 at mRNA and protein levels was detected by real-time fluorescence quantitative PCR and Western blotting. The luciferase assay was performed in HEK293T cells and CM cells, which were co-transfected with plasmid DNA and miRNA using Lipofectamine 2000. RESULTS: Transfection of miR-29a mimics significantly reduced the expression levels of Bcl-2 and Mcl-1 in CM cells as compared with the control cells (P<0.05). In addition, HEK293T cells co-transfected with miR-29a mimic and Bcl-2-3’UTR-WT or Mcl-1-3’UTR-WT plasmid significantly reduced the luciferase activity as compared with control group (P<0.05). While CM cells transfected with miR-29a inhibitor and Bcl-2-3’UTR-WT or Mcl-1-3’UTR-WT plasmid in succession, the luciferase activity was increased inversely (P<0.05). CONCLUSION: miR-29a may regulate apoptosis by targeting the bcl-2 and mcl-1 genes. 相似文献