蛋白磷酸酶2A癌性抑制剂在人三阴性乳腺癌中的表达与肿瘤生存、侵袭及自噬相关。
Expression of cancerous inhibitor of protein phosphatase 2A in human triple negative breast cancer correlates with tumor survival, invasion and autophagy.
作者信息
Li Shan, Feng Ting-Ting, Guo Yang, Yu Xianjun, Huang Qiuyue, Zhang Liang, Tang Wei, Liu Ying
机构信息
Department of Biochemistry, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.
School of Basic Medical Sciences, Anhui Medical University, Heifei, Anhui 230032, P.R. China.
出版信息
Oncol Lett. 2016 Dec;12(6):5370-5376. doi: 10.3892/ol.2016.5374. Epub 2016 Nov 9.
Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently characterized oncoprotein which is involved in the progression of several human malignancies. The present study aimed to investigate its biological function in human triple negative breast cancer (TNBC). The expression of CIP2A in TNBC cells was examined and it was observed that CIP2A was elevated in the TNBC cell line compared with poorly invasive breast cancer cells. CIP2A depletion in TNBC cell lines inhibited proliferation, and induced apoptosis and autophagy. In addition, CIP2A depletion inhibited invasion and migration of TNBC cells. Furthermore, CIP2A depletion downregulated Akt/mTOR/P70S6K phosphorylation. These results validate the role of CIP2A as a invasion-associated oncoprotein and established CIP2A as a promising therapeutic target of TNBC.
蛋白磷酸酶2A的癌性抑制剂（CIP2A）是一种最近被鉴定的癌蛋白，它参与多种人类恶性肿瘤的进展。本研究旨在探讨其在人类三阴性乳腺癌（TNBC）中的生物学功能。检测了TNBC细胞中CIP2A的表达，发现与低侵袭性乳腺癌细胞相比，TNBC细胞系中CIP2A表达升高。TNBC细胞系中CIP2A的缺失抑制了细胞增殖，并诱导了细胞凋亡和自噬。此外，CIP2A的缺失抑制了TNBC细胞的侵袭和迁移。此外，CIP2A的缺失下调了Akt/mTOR/P70S6K的磷酸化。这些结果证实了CIP2A作为一种与侵袭相关的癌蛋白的作用，并确立了CIP2A作为TNBC一个有前景的治疗靶点。
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