Open Access

ARTICLE

miR-767-3p Inhibits Growth and Migration of Lung Adenocarcinoma Cells by Regulating CLDN18

Yi Long Wan^*, Han Jue Dai^†, Wei Liu^‡, Hai Tao Ma^*

* Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China
† Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China
‡ Department of Cardiology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China

Oncology Research 2018, 26(4), 637-644. https://doi.org/10.3727/096504017X15112639918174

Abstract

Claudin18 (CLDN18) is necessary for intercellular junctions and is reported to be involved in cell migration and metastasis, making it like an oncogene in various cancer types. However, the biological function and regulatory mechanisms of CLDN18 in lung adenocarcinoma are not yet clear. In this study, we found downregulation of miR-767-3p and upregulation of CLDN18 in lung adenocarcinoma tissue and cell lines. In addition, there was a negative correlation between the expression of miR-767-3p and CLDN18 in lung adenocarcinoma. Double luciferase reporter gene analysis showed that miR-767-3p modulates the expression of CLDN18 by binding its 3'-untranslated regions (3'-UTR). Knockdown of CLDN18 results in a decrease in the growth, migration, and invasion of lung adenocarcinoma cells. Although overexpression of miR-767-3p inhibits lung adenocarcinoma cell growth and migration, these effects can be rescued by reexpressing CLDN18. In summary, the data suggest that miR-767-3p inhibits tumor cell proliferation, migration, and invasion by targeting CLDN18, providing a promising therapeutic target for lung adenocarcinoma.

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