4.4 Article

Ras-association domain family 1 (RASSF1A) gene regulates progression, migration and invasion of bladder cancer

Journal

SURGICAL ONCOLOGY-OXFORD
Volume 30, Issue -, Pages 63-71

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.suronc.2019.05.009

Keywords

Bladder cancer; RASSF1A; Migration; Invasion; Apoptosis

Funding

  1. Liaoning Province Scientific Projects [2013408001]

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Background: Bladder cancer is common malignant tumor around the world. Ras-association domain family 1 (RASSF1A) gene is inactivated in most of cancers. The aim of the study is to analyze the relationship between RASSF1A and the progression of bladder and investigate the effects of RASSF1A overexpression on bladder cancer cell in vitro. Materials and methods: Immunohistochemistry assay analyzed the RASSF1A expression in bladder tissue of bladder cancer patients. Besides, the data of 138 bladder cancer patients about RASSF1A expression was analyzed. Kaplan-Meier method analyzed the connection between disease free survival (DFS) and abnormal expression of RASSF1A and E-cadherin in bladder cancer patients. RASSF1A gene transfected the bladder cancer cells by lipofectamine. Cell proliferation was determined by methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis and cell cycle was detected using flow cytometry. Scratch assay evaluated cell migration, and transwell assay evaluated cell invasion. Western blot analyzed protein expression while qRT-PCR analyzed mRNA expression. Results: Bladder cancer tissues had lower RASSF1A expression compared with normal tissues, and the Patients with abnormal expression of RASSF1A had lower DFS and had higher possibility of recurrence and muscular layer infiltration. Besides, RASSF1A had significant difference with E-cadherin. RASSF1A overexpression inhibited the bladder cancer cell proliferation, migration and invasion, besides, it promoted apoptosis and the expression of E-cadherin and beta-catenin. Conclusion: RASSF1A may be a biomarker to evaluate the progression and recurrence of bladder cancer.

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