BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways.
BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways.
复制标题
BMX/Etk通过PI3K/AKT/mTOR和STAT3通路促进宫颈癌细胞增殖和致瘤
DOI：
10.18632/oncotarget.17493
复制
发表时间：
2017-07-25
期刊：
影响因子：
--
通讯作者：
Yang WT
中科院分区：
文献类型：
--
作者：
Li Y;Cui N;Zheng PS;Yang WT
骨髓X-连锁激酶（BMX，也称为Etk）已被报道参与多种类型肿瘤的细胞增殖、分化、凋亡、迁移和侵袭，但其在宫颈癌中的作用仍知之甚少。在本研究中，我们发现BMX表达呈现出从正常宫颈组织到宫颈原位癌，再到浸润性宫颈癌组织逐渐增加的趋势。BMX激酶抑制剂BMX-IN-1通过抑制BMX的表达，抑制细胞增殖。使用两种不同的沉默技术，TALEN和shRNA，在HeLa和SiHa宫颈癌细胞系中敲低BMX抑制体外细胞生长并抑制体内异种移植肿瘤形成，而在细胞系C-33 A中过表达BMX显著增加细胞增殖。进一步的机制研究表明，沉默BMX可阻断细胞周期从G 0/G1期向S期或G2/M期的转变，而敲低BMX可抑制p-AKT和p-STAT 3的表达。提示BMX可通过PI 3 K/AKT/mTOR和STAT 3信号通路促进宫颈癌细胞增殖。
Bone marrow X-linked kinase (BMX, also known as Etk) has been reported to be involved in cell proliferation, differentiation, apoptosis, migration and invasion in several types of tumors, but its role in cervical carcinoma remains poorly understood. In this study, we showed that BMX expression exhibits a gradually increasing trend from normal cervical tissue to cervical cancer in situ and then to invasive cervical cancer tissue. Through BMX-IN-1, a potent and irreversible BMX kinase inhibitor, inhibited the expression of BMX, the cell proliferation was significantly decreased. Knockdown of BMX in HeLa and SiHa cervical cancer cell lines using two different silencing technologies, TALEN and shRNA, inhibited cell growth in vitro and suppressed xenograft tumor formation in vivo, whereas overexpression of BMX in the cell line C-33A significantly increased cell proliferation. Furthermore, a mechanism study showed that silencing BMX blocked cell cycle transit from G0/G1 to S or G2/M phase, and knockdown of BMX inhibited the expression of p-AKT and p-STAT3. These results suggested that BMX can promote cell proliferation through PI3K/AKT/mTOR and STAT3 signaling pathways in cervical cancer cells.
登录
查看更多内容
影响因子：
5.2
作者：
Fritz, Rafael D.;Radziwill, Gerald
通讯作者：
Radziwill, Gerald
EZH2介导的GSK-3β和TP53抑制促进宫颈癌中Wnt/β-连环蛋白信号依赖性细胞扩增
影响因子：
--
作者：
Chen Q;Zheng PS;Yang WT
通讯作者：
Yang WT
影响因子：
56.9
作者：
Boch, Jens;Scholze, Heidi;Bonas, Ulla
通讯作者：
Bonas, Ulla
影响因子：
9.7
作者：
Engelbrecht, AM;Gebhardt, S;Louw, L
通讯作者：
Louw, L
影响因子：
3.6
作者：
Guo, Linlang;Chen, Pinglian;Sun, Yanqin
通讯作者：
Sun, Yanqin