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Research Paper|Volume 12, Issue 8|pp 6680—6699

Long intergenic non-protein coding RNA 324 prevents breast cancer progression by modulating miR-10b-5p

Bo Wang1, Yangyang Zhang1, Haitian Zhang2, Faquan Lin3, Qixin Tan4, Qinghong Qin4, Wei Bao1, Yi Liu1, Jiaying Xie1, Qiyan Zeng1
  • 1Department of Biochemistry and Molecular Biology, Guangxi Medical University, Nanning 530021, Guangxi, P.R. China
  • 2Department of Gastrointestinal and Gland Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi, P.R. China
  • 3Department of Clinical Laboratory, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi, P.R. China
  • 4Department of Breast Surgery, Guangxi Medical University Tumor Hospital, Nanning 530021, Guangxi, P.R. China
Received: November 27, 2019Accepted: March 3, 2020Published: April 18, 2020
https://doi.org/10.18632/aging.103021

Copyright © 2020 Wang 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

Mounting evidence suggests that long noncoding RNAs serve as specific biomarkers and potent modulators of multiple cancers. Long intergenic non-protein coding RNA 324 (LINC00324) is ubiquitously expressed in various tissues, including breast cancer. The biological function of LINC00324 in the development and progression of breast cancer remains unknown. Here, we fully elucidate the relation between LINC00324 expression and breast cancer, and suggest a potential mechanism of action. We found that decreased expression of LINC00324 was dramatically correlated with malignancy of breast cancer, both in breast cancer tissues and in cell lines. Overexpression of LINC00324 in MDA-MB-231 cells resulted in a decrease in cell proliferation, invasion, and migration, while increasing cells apoptosis. On the other hand, loss-of-function experiments indicated that deficiency of LINC00324 promoted malignant phenotypes in breast cancer cells. Mechanically, we found that LINC00324 is mainly distributed in the cytoplasm, fostering the expression of E-cadherin by sponging miR-10b-5p. Taken together, these findings suggest that LINC00324 plays a critical role in breast cancer progression by directly interacting with miR-10b-5p. LINC00324 can thus potentially act as an early diagnostic marker and a novel therapeutic agent for breast cancer.