MiR-133b regulates bladder cancer cell proliferation and apoptosis by targeting Bcl-w and Akt1.
MiR-133b regulates bladder cancer cell proliferation and apoptosis by targeting Bcl-w and Akt1.
复制标题
DOI：
10.1186/s12935-014-0070-3
复制
发表时间：
2014
影响因子：
5.8
通讯作者：
Wu B
中科院分区：
文献类型：
--
作者：
Chen XN;Wang KF;Xu ZQ;Li SJ;Liu Q;Fu DH;Wang X;Wu B
MiR-133 b是一种肌肉特异性microRNA，通过调节靶基因在心肌细胞的形成和心肌离子通道的表达中发挥作用。许多人类恶性肿瘤显示miR-133 b的低表达，如在结直肠癌、肺癌、食道癌和膀胱癌中所指出的，但miR-133 b在膀胱癌中的作用尚不清楚。采用茎环RT-PCR方法检测miR-133 b在膀胱癌组织及癌旁正常组织中的表达。同时分析miR-133 b表达与膀胱癌临床病理因素的关系。采用Western blot法检测41例膀胱癌组织及癌旁正常组织中Bcl-w和Akt 1蛋白的表达。将miR-133 b模拟物或抑制剂转染T24人膀胱癌细胞系后，分别通过Western blot和RT-PCR检测Bcl-w和Akt 1蛋白和mRNA的表达。CCK-8法检测miR-133 b对T24细胞增殖的影响，流式细胞术检测miR-133 b对T24细胞凋亡的影响。41例膀胱癌组织中miR-133 b的表达显著下调（P <0. 01），miR-133 b的低表达与膀胱癌的高分级密切相关（P <0. 01）。Bcl-w和Akt 1蛋白在膀胱癌组织中的表达显著高于癌旁正常组织（P < 0.01）。转染miR-133 b模拟物或抑制剂后，T24细胞Akt 1和Bcl-w蛋白及Akt 1 mRNA的表达分别显著下调或上调，而Bcl-w mRNA的表达无显著差异。用miR-133 b转染HEK-293 T细胞显著抑制了含有Bcl-w或Akt 1 3′-非翻译区的端粒酶报告基因。miR-133 b模拟物显著抑制T24细胞增殖，以及增加T24细胞凋亡（分别为P < 0.05和P < 0.01），而miR-133 b抑制剂分别增加和减少这些（两者均为P < 0.05）。miR-133 b可能通过调节Bcl-w和Akt 1的表达，在T24细胞的增殖和凋亡中发挥重要作用。
MiR-133b is a muscle-specific microRNA; it has a role in the formation of cardiocytes and the expression of myocardium ion channels by regulating target genes. Many human malignant tumors demonstrate a low expression of miR-133b, as noted in colorectal, lung, esophagus and bladder cancers, but the role of miR-133b in bladder cancer is unknown. The expression of miR-133b in clinical bladder cancer specimens and adjacent normal tissues was confirmed by stem-loop RT-PCR. We also analyzed the relationship between miR-133b expression and clinicopathological factors of bladder cancer. Bcl-w and Akt1 protein expression in 41 bladder cancer specimens and adjacent normal tissues was detected by Western blot. After transfection of miR-133b mimics or inhibitor into a T24 human bladder cancer cell line, Bcl-w and Akt1 protein and mRNA expression were examined by Western blot and RT-PCR, respectively. The effect of miR-133b on T24 cell proliferation and apoptosis was measured by CCK-8 tests and flow cytometry, respectively. The expression of miR-133b in bladder cancer tissues from 41 patients was significantly down-regulated (P < 0.01); low expression of miR-133b was strongly associated with high-grade bladder cancer (P < 0.01). Bcl-w and Akt1 proteins were significantly overexpressed in bladder cancer tissues versus adjacent normal tissues (P < 0.01 for both). The expression of Akt1 and Bcl-w proteins and Akt1 mRNA, in T24 cells was significantly down-regulated or up-regulated after transfection of miR-133b mimics or inhibitor, respectively; however, there was no significant difference in Bcl-w mRNA expression. Transfection of HEK-293 T cells with miR-133b significantly suppressed a luciferase-reporter containing the Bcl-w or Akt 1 3′-untranslated regions. MiR-133b mimics significantly inhibited T24 cell proliferation, as well as increased T24 cell apoptosis (P < 0.05 and P < 0.01, respectively) while the miR-133b inhibitor increased and decreased these, respectively (P < 0.05 for both). MiR-133b may play a very important role in the proliferation and apoptosis of T24 cells by regulating the expression of Bcl-w and Akt1.
登录
查看更多内容
DOI：
10.1523/jneurosci.3347-10.2011
发表时间：
2011-02-02
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Courchesne SL;Karch C;Pazyra-Murphy MF;Segal RA
通讯作者：
Segal RA
影响因子：
5.1
作者：
Hummel, Richard;Maurer, Jessica;Haier, Joerg
通讯作者：
Haier, Joerg
影响因子：
8.8
作者：
通讯作者：
--
影响因子：
11.1
作者：
Lin, Pei-Ying;Yang, Pan-Chyr
通讯作者：
Yang, Pan-Chyr
影响因子：
37.3
作者：
Bandrés E;Cubedo E;Agirre X;Malumbres R;Zárate R;Ramirez N;Abajo A;Navarro A;Moreno I;Monzó M;García-Foncillas J
通讯作者：
García-Foncillas J