MiR-650 represses high-risk non-metastatic colorectal cancer progression via inhibition of AKT2/GSK3β/E-cadherin pathway.
MiR-650 represses high-risk non-metastatic colorectal cancer progression via inhibition of AKT2/GSK3β/E-cadherin pathway.
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MiR-650 通过抑制 AKT2/GSK3β/E-钙粘蛋白途径抑制高风险非转移性结直肠癌进展
DOI:
10.18632/oncotarget.17743
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发表时间:
2017-07-25
期刊:
影响因子:
--
通讯作者:
Wang S
中科院分区:
文献类型:
--
作者:
Zhou C;Cui F;Li J;Wang D;Wei Y;Wu Y;Wang J;Zhu H;Wang S
Although 5-year survival rate of non-metastatic colorectal cancer (CRC) is high, about 10% of patients in stage I and II still develop into metastatic CRC and eventually die after resection. Currently, there is no effective biomarker for predicting the prognosis of non-metastatic CRC in clinical practice. In this study, we identified miR-650 as a biomarker for prognosis prediction. We observed that the expression of miR-650 in tumor tissues had a positive association with overall survival. MiR-650 inhibited cell growth and invasion in vitro and in vivo. Furthermore, miR-650 targeted AKT2 and repressed the activation of the AKT pathway (AKT2/GSK3β/E-cadherin). Thus it induced the translocation of E-cadherin and β-catenin in cancer cells. Our results highlight the potential of miR-650 as a prognostic prediction biomarker and therapeutic target in non-metastatic CRC via inhibition of the AKT2/GSK3β/E-cadherin pathway.
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影响因子:
6.4
作者:
Oue, Naohide;Anami, Katsuhiro;Schetter, Aaron J.;Moehler, Markus;Okayama, Hirokazu;Khan, Mohammed A.;Bowman, Elise D.;Mueller, Annett;Schad, Arno;Shimomura, Manabu;Hinoi, Takao;Aoyagi, Kazuhiko;Sasaki, Hiroki;Okajima, Masazumi;Ohdan, Hideki;Galle, Peter R.;Yasui, Wataru;Harris, Curtis C.
通讯作者:
Harris, Curtis C.
DOI:
10.1073/pnas.0810715105
发表时间:
2008-12-23
影响因子:
11.1
作者:
Rychahou, Piotr G.;Kang, JungHee;Evers, B. Mark
通讯作者:
Evers, B. Mark
影响因子:
120.7
作者:
Schetter, Aaron J.;Leung, Suet Yi;Harris, Curtis C.
通讯作者:
Harris, Curtis C.
影响因子:
4.4
作者:
Wang S;Wang L;Zhu T;Gao X;Li J;Wu Y;Zhu H
通讯作者:
Zhu H
影响因子:
5.2
作者:
Akcakaya, Pinar;Ekelund, Susanne;Lui, Weng-Onn
通讯作者:
Lui, Weng-Onn