Open AccessPTEN/AKT upregulation of TMSB10 contributes to lung cancer cell growth and predicts poor survival of the patients
Author(s) -
Jie Li,
Shaohui Zhou,
Hongchen Li,
Yanzhao Xu,
Ning Zhou,
Rongfeng Liu
Publication year - 2020
Publication title -
bioscience biotechnology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.509
H-Index - 116
eISSN - 1347-6947
pISSN - 0916-8451
DOI - 10.1093/bbb/zbaa113
Subject(s) - pten , protein kinase b , cancer research , lung cancer , oncogene , downregulation and upregulation , cancer , gene knockdown , carcinogenesis , pi3k/akt/mtor pathway , epithelial–mesenchymal transition , cell growth , signal transduction , biology , medicine , oncology , apoptosis , cell cycle , metastasis , microbiology and biotechnology , biochemistry , genetics , gene
PTEN/AKT signaling cascade is frequently activated in various cancers, including lung cancer. The downstream effector of this signaling cascade is poorly understood. β-Thymosin 10 (TMSB10) functions as an oncogene or tumor suppressors in cancers, whereas its significance in lung cancer remains unknown. In this study, we showed that the activation of PTEN/AKT signaling promoted the expression of TMSB10. Based on the TCGA database, TMSB10 was upregulated in lung cancer tissues and its overexpression was correlated with poor prognosis of lung cancer patients. Functional experiments demonstrated that TMSB10 knockdown suppressed, while its overexpression promoted the proliferation, growth, and migration of lung cancer cells. Apoptosis and epithelial-mesenchymal transition were also regulated by TMSB10. We therefore suggest that TMSB10 is a novel oncogene for lung cancer. Targeting TMSB10 may benefit lung cancer patients with activated PTEN/AKT signaling.
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