Open AccessKnockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non‑small cell lung cancer via the regulation of epithelial‑to‑mesenchymal transition
Author(s) -
Xiang Xu,
Hanwen Zhu,
Minglei Yang,
Enkuo Zheng,
Ye Zhou,
Junjun Ni,
Rui Li,
Zhenhua Yang,
Tao He,
Guofang Zhao
Publication year - 2019
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2019.8358
Subject(s) - gene knockdown , vimentin , epithelial–mesenchymal transition , cancer research , biology , gene silencing , metastasis , lung cancer , regulator , cell cycle , a549 cell , cancer , oncology , medicine , cell culture , immunohistochemistry , immunology , gene , biochemistry , genetics
Non-small cell lung cancer (NSCLC) is one of the most common cancer types worldwide. Previous studies have indicated that TOR signaling pathway regulator (TIPRL) is involved in the progression of NSCLC. However, the underlying mechanisms of the role of TIPRL in regulating NSCLC metastasis have remained largely elusive. In the present study, the expression pattern of TIPRL in NSCLC was analyzed using The Cancer Genome Atlas (TCGA) dataset. Furthermore, Kaplan-Meier curve analysis was performed to evaluate the prognostic value of TIPRL in NSCLC, using the Kaplan-Meier Plotter and TCGA datasets. Loss-of-function assays were performed to determine the effects of TIPRL on cell migration and invasion. The results suggested that TIPRL was upregulated in NSCLC and positively associated with an advanced Tumor-Node-Metastasis stage. A higher expression level of TIPRL was associated with shorter overall and disease-free survival times in patients with NSCLC. To the best of our knowledge, the present study was the first to report that TIPRL acts as a metastasis promoter in NSCLC. Silencing of TIPRL suppressed A549 cell migration and invasion. Mechanistically, the present study indicated that TIPRL knockdown significantly promoted epithelial-cadherin expression, whereas it suppressed twist and vimentin expression in A549 cells. In conclusion, the present analysis suggested that TIPRL may serve as a biomarker for the prognosis of NSCLC and as a future target for its treatment.