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Knockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non-small cell lung cancer via the regulation of epithelial-to-mesenchymal transition.

ABSTRACT: 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.

SUBMITTER: Xu X

PROVIDER: S-EPMC7027157 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Knockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non-small cell lung cancer via the regulation of epithelial-to-mesenchymal transition.

Xu Xiang X Zhu Huangkai H Yang Minglei M Zheng Enkuo E Zhou Yinjie Y Ni Junjun J Li Rui R Yang Zhenhua Z He Ti T Zhao Guofang G

Experimental and therapeutic medicine 20191220 3

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 ...[more]

PMID: 32104250

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Project description:ObjectiveInhibition of tumor metastasis is a useful strategy to improve the efficacy of cancer therapy. Ventilagolin, a natural 1, 4-naphthoquinone derivative extracted from Ventilago leiocarpa Benth, has shown promising antitumor effects in previous studies. However, the effects and underlying mechanisms of Ventilagolin against migration, invasion and epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma (HCC) remain unclear. The present study has examined these effects and determined whether the proto-oncogene Pim-1 is involved.MethodsThe effects of Ventilagolin on migration, invasion, Pim-1 and EMT-related proteins (eg, E-cadherin, N-cadherin, Vimentin) expression were assessed by scratch wound healing, Transwell, qRT-PCR and Western blot assays, respectively. Pim-1 stably overexpressed HepG2 and SMMC-7721 cells were generated to explore whether Ventilagolin inhibited migration, invasion and EMT of HCC cells via regulating Pim-1. Subcutaneous xenograft tumor model in nude mice was established. Histopathological changes of tumor tissues were examined by H&E staining and expressions of Pim-1 and EMT-related proteins were detected by immunohistochemistry.ResultsVentilagolin significantly (P < 0.01) reduced the expression of Pim-1 levels in HepG2 and SMMC-7721 cells. Compared with the control group, the migration and invasion abilities of Pim-1-overexpressing HepG2 and SMMC-7721 cells were significantly (P < 0.05, P < 0.01) enhanced, the expression of E-cadherin was decreased (P < 0.01), and the levels of N-cadherin and Vimentin were upregulated (P < 0.05, P < 0.01). Ventilagolin treatment effectively reversed these effects of Pim-1 overexpression. In vivo experiments showed that Ventilagolin could effectively suppress HCC tumor growth, downregulate Pim-1, N-cadherin and Vimentin expression, and upregulate E-cadherin expression.ConclusionVentilagolin suppresses HCC cell proliferation, migration and invasion and reverses EMT process by downregulating Pim-1, suggesting Ventilagolin is a potential therapeutic agent for treatment of HCC.

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Knockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non-small cell lung cancer via the regulation of epithelial-to-mesenchymal transition.

Publications

Knockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non-small cell lung cancer via the regulation of epithelial-to-mesenchymal transition.

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