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Research Paper|Volume 13, Issue 4|pp 6010—6024

Exosomal long non-coding RNA LINC00662 promotes non-small cell lung cancer progression by miR-320d/E2F1 axis

Xin Lv1, Yingjie Lian2, Zhanye Liu2, Jianguang Xiao3, Donghua Zhang4, Xiaohua Yin5
  • 1Department of Respiratory and Critical Care Medicine, Linyi People's Hospital, Linyi, Shandong Province, China
  • 2Department of Thoracic Surgery, Cao County People’s Hospital, Heze, Shandong Province, China
  • 3Department of Thoracic Surgery, Laizhou People’s Hospital, Laizhou, Shandong Province, China
  • 4Department of Oncology, Zhangqiu People’s Hospital, Zhangqiu, Shandong Province, China
  • 5Department of Traditional Chinese Medicine, Shengli Oil Field Central Hospital, Dongying, Shandong Province, China
* Equal contribution
Received: August 26, 2020Accepted: November 13, 2020Published: February 11, 2021
https://doi.org/10.18632/aging.202522

Copyright: © 2021 Lv et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Non-small cell lung cancer (NSCLC) is the most common tumor affecting modern people and is associated with severe morbidity and high mortality. Exosomal long non-coding RNAs as crucial regulators are involved in cancer progression. However, the role of exosomal lncRNA LINC00662 in the development of NSCLC remains unclear. Here, we aimed to explore the impact of exosomal lncRNA LINC00662 on the NSCLC progression and the underlying mechanism. Significantly, we revealed that the expression of lncRNA LINC00662 was elevated in the plasma exosome of NSCLC patients. Exosomal LINC00662 promoted proliferation, invasion, and migration, and inhibited apoptosis and cell cycle arrest of NSCLC cells. Mechanically, LINC00662 was able to serve as a miR-320d sponge in NSCLC cells. MiR-320d could target E2F1 in NSCLC cells. Exosomal LINC00662 contributed to the progression of NSCLC by miR-320d/E2F1 axis in vitro. Remarkably, exosomal LINC00662 enhanced the tumor growth of NSCLC in vivo. Thus, we conclude that exosomal lncRNA LINC00662 promotes NSCLC progression by modulating miR-320d/E2F1 axis. Our finding provides new insights into the mechanism by which exosomal lncRNA LINC00662 contributes to the development of NSCLC. LncRNA LINC00662, miR-320d, and E2F1 may serve as potential targets for NSCLC therapy.