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VGLL4 Selectively Represses YAP-Dependent Gene Induction and Tumorigenic Phenotypes in Breast Cancer.VGLL4 选择性抑制乳腺癌中 YAP 依赖性基因诱导和肿瘤表型。
Sci Rep. 2017 Jul 21;7(1):6190. doi: 10.1038/s41598-017-06227-7.
2
Review of hepatocellular carcinoma: Epidemiology, etiology, and carcinogenesis.肝细胞癌综述:流行病学、病因学与致癌机制
J Carcinog. 2017 May 29;16:1. doi: 10.4103/jcar.JCar_9_16. eCollection 2017.
3
HtrA1 Down-regulation Induces Cisplatin Resistance in Colon Cancer by Increasing XIAP and Activating PI3K/Akt Pathway.HtrA1下调通过增加XIAP和激活PI3K/Akt通路诱导结肠癌顺铂耐药。
Ann Clin Lab Sci. 2017 May;47(3):264-270.
4
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Mol Cell Oncol. 2017 Feb 25;4(3):e1295127. doi: 10.1080/23723556.2017.1295127. eCollection 2017.
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Personalized therapy in hepatocellular carcinoma: Molecular markers of prognosis and therapeutic response.肝细胞癌的个性化治疗:预后和治疗反应的分子标志物
Surg Oncol. 2017 Jun;26(2):138-145. doi: 10.1016/j.suronc.2017.01.009. Epub 2017 Feb 21.
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Rab11a promotes proliferation and invasion through regulation of YAP in non-small cell lung cancer.Rab11a通过调控YAP促进非小细胞肺癌的增殖和侵袭。
Oncotarget. 2017 Apr 25;8(17):27800-27811. doi: 10.18632/oncotarget.15359.
8
Small nucleolar RNA ACA11 promotes proliferation, migration and invasion in hepatocellular carcinoma by targeting the PI3K/AKT signaling pathway.小核仁 RNA ACA11 通过靶向 PI3K/AKT 信号通路促进肝癌的增殖、迁移和侵袭。
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YAP的下调抑制人肝癌细胞的增殖、侵袭并增加顺铂敏感性。

Downregulation of YAP inhibits proliferation, invasion and increases cisplatin sensitivity in human hepatocellular carcinoma cells.

作者信息

Wang Xiaoguang, Wu Bin, Zhong Zhengxiang

机构信息

Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Jiaxing Medical College, Jiaxing, Zhejiang 314000, P.R. China.

出版信息

Oncol Lett. 2018 Jul;16(1):585-593. doi: 10.3892/ol.2018.8633. Epub 2018 May 4.

DOI:10.3892/ol.2018.8633
PMID:29928445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6006453/
Abstract

Yes-associated protein (YAP) serves an essential role in tumorigenesis. However, the potential role and the molecular mechanism underlying the effect of YAP on hepatocellular carcinoma (HCC) cells have not been elucidated. In the current study, it was revealed that YAP expression was increased significantly in HCC cancer tissues and its overexpression was associated with tumor differentiation. The silencing of YAP by small interferring RNA led to the inhibition of HCC cell growth, which was associated with the promotion of apoptosis. The silencing of YAP also decreased the invasive potential of HCC cells and the activity of the phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase (AKT) signaling pathway. Furthermore, silencing of YAP increased the chemosensitivity of HCC cells to cisplatin (CDDP) through inactivation of the PI3K/AKT signaling pathway. studies using PDTX model suggested a promotive role for YAP in the growth of HCC and knockdown of YAP increased the anti-tumor activity of CDDP. Taken together, these results revealed that YAP is overexpressed in HCC, and promotes proliferation, invasion and drug resistance of HCC cells. Inhibition of YAP, alone or in combination with traditional chemotherapy, may effectively combat HCC.

摘要

Yes相关蛋白(YAP)在肿瘤发生过程中发挥着重要作用。然而,YAP对肝癌(HCC)细胞作用的潜在作用及分子机制尚未阐明。在本研究中,发现YAP在肝癌组织中表达显著增加,其过表达与肿瘤分化相关。小干扰RNA沉默YAP导致肝癌细胞生长受到抑制,这与细胞凋亡的促进有关。YAP的沉默还降低了肝癌细胞的侵袭能力以及磷酸肌醇3激酶(PI3K)/AKT丝氨酸/苏氨酸激酶(AKT)信号通路的活性。此外,YAP的沉默通过使PI3K/AKT信号通路失活增加了肝癌细胞对顺铂(CDDP)的化疗敏感性。使用人源肿瘤异种移植(PDTX)模型的研究表明YAP在肝癌生长中起促进作用,敲低YAP可增强CDDP的抗肿瘤活性。综上所述,这些结果表明YAP在肝癌中过表达,并促进肝癌细胞的增殖、侵袭和耐药性。抑制YAP,单独或与传统化疗联合使用,可能有效对抗肝癌。