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首页> 外文期刊>Oncology letters >Expression of cancerous inhibitor of protein phosphatase 2A in human triple negative breast cancer correlates with tumor survival, invasion and autophagy
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Expression of cancerous inhibitor of protein phosphatase 2A in human triple negative breast cancer correlates with tumor survival, invasion and autophagy

机译: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的生存,侵袭和自噬有关

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摘要

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 promiing therapeutic target of TNBC.
机译:蛋白磷酸酶2A(CIP2A)的癌性抑制剂是最近表征的癌蛋白,它参与了几种人类恶性肿瘤的发展。本研究旨在调查其在人类三阴性乳腺癌(TNBC)中的生物学功能。检查了CIP2A在TNBC细胞中的表达,并且观察到与侵袭性差的乳腺癌细胞相比,CIP2A在TNBC细胞系中升高。 TNBC细胞系中的CIP2A消耗抑制增殖,并诱导凋亡和自噬。此外,CIP2A耗竭抑制TNBC细胞的侵袭和迁移。此外,CIP2A消耗下调Akt / mTOR / P70S6K磷酸化。这些结果验证了CIP2A作为入侵相关癌蛋白的作用,并确定了CIP2A作为TNBC的重要治疗靶标。

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