Open Access

CORRECTION

MicroRNA-133a Inhibits Proliferation of Gastric Cancer Cells by Downregulating ERBB2 Expression

Chang Li^*, Xiaoping Li^†, Shuohui Gao^*, Chang Li^‡, Lianjun Ma^§

* Department of Gastrointestinal Internal Medicine, China–Japan Union Hospital of Jilin University, Changchun, P.R. China
† Department of Pediatrics, The First Hospital of Jilin University, Changchun, P.R. China
‡ Department of Cadre’s Ward, China–Japan Union Hospital of Jilin University, Changchun, P.R. China
§ Endoscopy Center, China–Japan Union Hospital of Jilin University, Changchun, P.R. China

Oncology Research 2020, 28(7-8), 819-822. https://doi.org/10.3727/096504021X16240202940003

Abstract

Gastric cancer is the fourth most common type of cancer and the second highest leading cause of cancer-related deaths worldwide. It has already been established that miR-133a is involved in gastric cancer. In this study, we investigated the molecular mechanisms by which miR-133a inhibits the proliferation of gastric cancer cells. We analyzed the proliferative capacity of human gastric cancer cells SNU-1 using an MTT assay. Cell apoptosis was determined using flow cytometry. The expression levels of ERBB2, p-ERK1/2, and p-AKT in SNU-1 cells were determined using Western blot analysis. To confirm that ERBB2 is a direct target of miR-133a, a luciferase reporter assay was performed. Results showed that miR-133a overexpression inhibited SNU-1 cell proliferation and increased apoptosis. ERBB2 was a direct target of miR-133a, and it was negatively regulated by miR-133a. Interestingly, ERBB2 silencing has a similar impact to miR-133a overexpression, in that it significantly induced apoptosis and inhibited ERK and AKT activation. Our study showed that miR-133a inhibits the proliferation of gastric cancer cells by downregulating the expression of ERBB2 and its downstream signaling molecules p-ERK1/2 and p-AKT. Therefore, miR-133a might be used as a therapeutic target for treating gastric cancer.

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