目的:探讨miR-129-5p通过调控高迁移率族蛋白B1基因(high mobility group box 1,HMGB1)影响乳腺癌MCF-7细胞对紫杉醇(paclitaxel,PTX)的敏感性。方法:采用脂质体转染技术将miR-129-5p mimics、HMGB1小干扰RNA(si-HMGB1)分别转染入MCF-7...目的:探讨miR-129-5p通过调控高迁移率族蛋白B1基因(high mobility group box 1,HMGB1)影响乳腺癌MCF-7细胞对紫杉醇(paclitaxel,PTX)的敏感性。方法:采用脂质体转染技术将miR-129-5p mimics、HMGB1小干扰RNA(si-HMGB1)分别转染入MCF-7细胞,用PTX刺激培养细胞后,用实时荧光定量PCR检测转染后MCF-7细胞miR-129-5p和HMGB1 m RNA的表达,Western blotting检测转染后MCF-7细胞HMGB1蛋白的表达,CCK-8增殖实验检测转染后PTX对MCF-7细胞增殖的影响,流式细胞术检测转染后对PTX诱导MCF-7细胞凋亡的影响。结果:转染miR-129-5p mimics后,MCF-7细胞中miR-129-5p的表达水平明显高于阴性对照组细胞(P<0.01);过表达miR-129-5p后可明显增强PTX抑制MCF-7细胞的增殖和诱导细胞凋亡的能力(均P<0.05),并显著抑制HMGB1 m RNA和蛋白的表达(均P<0.05)。转染si-HMGB1后,显著降低MCF-7细胞HMGB1 m RNA和蛋白的表达(均P<0.05);干扰HMGB1表达进一步促进PTX抑制MCF-7细胞的增殖并诱导细胞凋亡(均P<0.05)。结论:miR-129-5p通过下调HMGB1的表达增强乳腺癌MCF-7细胞对PTX的敏感性。展开更多
AIM To investigate the role of long noncoding RNA(lnc RNA) RP4 in colorectal cancer.METHODS Lentivirus-mediated lnc RNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell pr...AIM To investigate the role of long noncoding RNA(lnc RNA) RP4 in colorectal cancer.METHODS Lentivirus-mediated lnc RNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting kit-8 assay, an in vivo xenograft tumor model, and annexin V/propidium iodide staining, respectively. Analysis of the lnc RNA RP4 mechanism involved assessment of the association of its expression with mi R-7-5 p and the SH3 GLB1 gene. Western blot analysis was also performed to assess the effect of lnc RNA RP4 on the autophagy-mediated cell death pathway and phosphatidylinositol-3-kinase(PI3 K)/Akt signaling.RESULTS Cell proliferation, tumor growth, and early apoptosis in SW480 cells were negatively regulated by lnc RNA RP4. Functional experiments indicated that lnc RNA RP4 directly upregulated SH3 GLB1 expression by acting as a competing endogenous RNA(ce RNA) for mi R-7-5 p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3 K and Akt phosphorylation in colorectal cancer cells in vivo.CONCLUSION Our results demonstrated that lnc RNA RP4 is a ce RNA that plays an important role in the pathogenesis of colorectal cancer, and could be a potential therapeutic target for colorectal cancer treatment.展开更多
文摘目的:探讨miR-129-5p通过调控高迁移率族蛋白B1基因(high mobility group box 1,HMGB1)影响乳腺癌MCF-7细胞对紫杉醇(paclitaxel,PTX)的敏感性。方法:采用脂质体转染技术将miR-129-5p mimics、HMGB1小干扰RNA(si-HMGB1)分别转染入MCF-7细胞,用PTX刺激培养细胞后,用实时荧光定量PCR检测转染后MCF-7细胞miR-129-5p和HMGB1 m RNA的表达,Western blotting检测转染后MCF-7细胞HMGB1蛋白的表达,CCK-8增殖实验检测转染后PTX对MCF-7细胞增殖的影响,流式细胞术检测转染后对PTX诱导MCF-7细胞凋亡的影响。结果:转染miR-129-5p mimics后,MCF-7细胞中miR-129-5p的表达水平明显高于阴性对照组细胞(P<0.01);过表达miR-129-5p后可明显增强PTX抑制MCF-7细胞的增殖和诱导细胞凋亡的能力(均P<0.05),并显著抑制HMGB1 m RNA和蛋白的表达(均P<0.05)。转染si-HMGB1后,显著降低MCF-7细胞HMGB1 m RNA和蛋白的表达(均P<0.05);干扰HMGB1表达进一步促进PTX抑制MCF-7细胞的增殖并诱导细胞凋亡(均P<0.05)。结论:miR-129-5p通过下调HMGB1的表达增强乳腺癌MCF-7细胞对PTX的敏感性。
基金Supported by Scientific Research Foundation of Anhui Education Department,No.KJ2017A219 to Liu MLScientific Research Foundation of Academic Leader of Anhui Province,No.2016H105 to Liu ML+2 种基金Education Talent Foundation of Universities of Anhui Education Department,No.gxbj ZD2016070 to Liu MLNational Natural Science Foundation of China,No.81500373 to Wang WBNatural Science Foundation of Anhui Province,No.1608085MH193 to Wang WB
文摘AIM To investigate the role of long noncoding RNA(lnc RNA) RP4 in colorectal cancer.METHODS Lentivirus-mediated lnc RNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting kit-8 assay, an in vivo xenograft tumor model, and annexin V/propidium iodide staining, respectively. Analysis of the lnc RNA RP4 mechanism involved assessment of the association of its expression with mi R-7-5 p and the SH3 GLB1 gene. Western blot analysis was also performed to assess the effect of lnc RNA RP4 on the autophagy-mediated cell death pathway and phosphatidylinositol-3-kinase(PI3 K)/Akt signaling.RESULTS Cell proliferation, tumor growth, and early apoptosis in SW480 cells were negatively regulated by lnc RNA RP4. Functional experiments indicated that lnc RNA RP4 directly upregulated SH3 GLB1 expression by acting as a competing endogenous RNA(ce RNA) for mi R-7-5 p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3 K and Akt phosphorylation in colorectal cancer cells in vivo.CONCLUSION Our results demonstrated that lnc RNA RP4 is a ce RNA that plays an important role in the pathogenesis of colorectal cancer, and could be a potential therapeutic target for colorectal cancer treatment.
