Abstract

Aberrant microRNA expression is involved in the regulation of various cellular processes, such as proliferation and metastasis in multiple diseases including cancers. MicroRNA‐30e‐5p (miR‐30e) was previously reported as an oncogenic or tumour suppressing miRNA in some malignancies, but its function in lung adenocarcinoma (LAC) remains largely undefined. In this study, we found that the expression of miR‐30e was increased in LAC tissues and cell lines, associated with tumour size and represented an independent prognostic factor for overall survival and recurrence of LAC patients. Further functional experiments showed that knockdown of miR‐30e suppressed cell growth while its overexpression promoted growth of LAC cells and xenografts in vitro and in vivo. Mechanistically, PTPN13 was identified as the direct target of miR‐30e in LAC, in which PTPN13 expression was down‐regulated in LAC tissues and showed the inverse correlation with miR‐30e expression. Overexpression of PTPN13 inhibited cell growth and rescued the proliferation‐promoting effect of miR‐30e through inhibition of the EGFR signalling. Altogether, our findings suggest that miR‐30e could function as an oncogene in LAC via targeting PTPN13 and act as a potential therapeutic target for treating LAC.

Highlights

  • Lung cancer is presently the leading cause of cancer deaths worldwide with the highest mortality rate [1]

  • The functions and molecular regulatory mechanisms of miR-30e in lung adenocarcinoma (LAC) remain unknown, in this study, we found that miR-30e expression was increased in LAC tissues and cell lines and indicated poor survival and recurrence in LAC patients

  • We further investigated the correlation between miR-30e expression and overall survival (OS) and recurrence in LAC patients using Kaplan–Meier and multivariate analysis, which indicated that miR-30e expression was the independent prognostic factor for the Overall survival (OS) (P = 0.024, Table S3) and recurrence (P = 0.036, Table S4) in LAC patients

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Summary

Introduction

Lung cancer is presently the leading cause of cancer deaths worldwide with the highest mortality rate [1]. Non-small cell lung cancer (NSCLC) including the LAC accounts for approximately 80% of lung cancer cases [2]. Based on different tumour histopathological types, miR-30e showed differential expression in different cancer types. In spite of a small amount of data displaying the decreased expression of miR-30e in NSCLC [13, 14], increasing evidence showed miR-30e was up-regulated in cancers including LAC [11] and exerted the oncogenic role in cancer [10, 12]. The functions and molecular regulatory mechanisms of miR-30e in LAC remain unknown, in this study, we found that miR-30e expression was increased in LAC tissues and cell lines and indicated poor survival and recurrence in LAC patients.

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