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PTBP1 promotes the growth of breast cancer cells through the PTEN/Akt pathway and autophagy

癌症研究 张力素 PTEN公司 生物 蛋白激酶B 癌变 PI3K/AKT/mTOR通路 多嘧啶结合蛋白 转移 乳腺癌 癌症 信号转导 细胞生物学 RNA结合蛋白 核糖核酸 遗传学 基因
作者
Xu Wang,Li Yang,Yan Fan,Xinmiao Yu,Xiaoyun Mao,Feng Jin
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:233 (11): 8930-8939 被引量:81
标识
DOI:10.1002/jcp.26823
摘要

Invasion and migration is the hallmark of malignant tumors as well as the major cause for breast cancer death. The polypyrimidine tract binding, PTB, protein serves as an important model for understanding how RNA binding proteins affect proliferation and invasion and how changes in the expression of these proteins can control complex programs of tumorigenesis. We have investigated some roles of polypyrimidine tract binding protein 1 (PTBP1) in human breast cancer. We found that PTBP1 was upregulated in breast cancer tissues compared with normal tissues and the same result was confirmed in breast cancer cell lines. Knockdown of PTBP1 substantially inhibited tumor cell growth, migration, and invasion. These results suggest that PTBP1 is associated with breast tumorigenesis and appears to be required for tumor cell growth and maintenance of metastasis. We further analyzed the relationship between PTBP1 and clinicopathological parameters and found that PTBP1 was correlated with her‐2 expression, lymph node metastasis, and pathological stage. This will be a novel target for her‐2( + ) breast cancer. PTBP1 exerts these effects, in part, by regulating the phosphatase and tensin homolog‐phosphatidylinositol‐4,5‐bisphosphate 3‐kinase/protein kinase B (PTEN‐PI3K/Akt) pathway and autophagy, and consequently alters cell growth and contributes to the invasion and metastasis.

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