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ROR1‐AS1 knockdown inhibits growth and invasion and promotes apoptosis in NSCLC cells by suppression of the PI3K/Akt/mTOR pathway
Author(s) -
Li Fengbo,
Gu Fengming,
Li Qian,
Zhai Chaoshuan,
Gong Rui,
Zhu Xuezhuan
Publication year - 2021
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22726
Subject(s) - pi3k/akt/mtor pathway , gene knockdown , apoptosis , protein kinase b , viability assay , cancer research , cell growth , chemistry , rptor , biology , biochemistry
Abstract The role of ROR1‐AS1 in non‐small‐cell lung cancer (NSCLC) remains unclear. Therefore, we aimed to investigate the functional role of ROR1‐AS1 in NSCLC and to explore the underlying mechanisms. 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide assay was performed to detect cell proliferation. Transwell assay was performed to evaluate cell invasive ability. Cell apoptotic rates and caspase‐3/7 activity were determined to evaluate apoptosis. The expression levels of PI3K/Akt/mTOR pathway‐related proteins were measured using Western blot analysis. Results showed that ROR1‐AS1 expression was upregulated in NSCLC samples. Knockdown of ROR1‐AS1 inhibited the viability and invasive ability of NSCLC cells. Knockdown of ROR1‐AS1 induced apoptotic rate and caspase‐3/7 activity and suppressed xenograft NSCLC tumor growth. In addition, ROR1‐AS1 knockdown inhibited the activation of the PI3K/Akt/mTOR pathway in NSCLC cells. However, treatment with 740Y‐P prevented the effects of si‐ROR1‐AS1 on viability, invasive ability, and apoptosis of NSCLC cells. These findings implied that ROR1‐AS1 played an oncogenic role in NSCLC via regulating the PI3K/Akt/mTOR pathway.