STK17B promotes carcinogenesis and metastasis via AKT/GSK-3β/Snail signaling in hepatocellular carcinoma.
STK17B promotes carcinogenesis and metastasis via AKT/GSK-3β/Snail signaling in hepatocellular carcinoma.
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STK17B 通过 AKT/GSK-3β/Snail 信号传导促进肝细胞癌的癌变和转移。
DOI:
10.1038/s41419-018-0262-1
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发表时间:
2018-02-14
影响因子:
9
通讯作者:
Liu L
中科院分区:
文献类型:
--
作者:
Lan Y;Han J;Wang Y;Wang J;Yang G;Li K;Song R;Zheng T;Liang Y;Pan S;Liu X;Zhu M;Liu Y;Meng F;Mohsin M;Cui Y;Zhang B;Subash S;Liu L
Hepatocellular carcinoma (HCC) is a lethal malignancy worldwide with frequent intrahepatic and distant metastasis. Elucidating the underlying molecular mechanism that modulates HCC progression is critical for exploring novel therapeutic strategies. Serine/Threonine Kinase 17B (STK17B) is upregulated in HCC tissues, but its role in HCC progression remains elusive. In the present studies, we reported that STK17B had a critical role in HCC progression. STK17B was significantly upregulated in HCC cell lines and specimens, and patients with ectopic STK17B expression characterized with poor clinicopathological features. In vitro and in vivo assay demonstrated that inhibition of STK17B markedly inhibits HCC tumorigenesis and metastasis, while STK17B overexpression promoted these processes. Furthermore, we found that STK17B promoted EMT process via activating AKT/GSK-3β/Snail signal pathway, and miR-455-3p was identified as the upstream regulator of STK17B. Combination of high level of STK17B and low level of miR-455-3p predicted poor prognosis with higher accuracy for HCC patients. In conclusion, our research demonstrated that STK17B promotes HCC progression, induces EMT process via activating AKT/GSK-3β/Snail signal and predicts poor prognosis in HCC.
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影响因子:
3.7
作者:
Liang Y;Yin D;Hou L;Zheng T;Wang J;Meng X;Lu Z;Song X;Pan S;Jiang H;Liu L
通讯作者:
Liu L
影响因子:
2.7
作者:
Jung, Myoung Eun;Byun, Byung Jin;Choi, Gildon
通讯作者:
Choi, Gildon
DOI:
10.1007/978-1-4419-0711-0_2
发表时间:
2010-01-01
期刊:
CANCER GENOME AND TUMOR MICROENVIRONMENT
影响因子:
--
作者:
Bellacosa, A.;Larue, L.
通讯作者:
Larue, L.
DOI:
10.1016/j.biocel.2017.07.023
发表时间:
2017-09-01
影响因子:
4
作者:
Wu, Yanjiao;Xu, Xiaoli;Tang, Liling
通讯作者:
Tang, Liling
影响因子:
13.5
作者:
Liu, Lulu;Dai, Yongdong;Guan, Xin-Yuan
通讯作者:
Guan, Xin-Yuan