Targeting of TLE3 by miR-3677 in human breast cancer promotes cell proliferation, migration and invasion.

Oncol Lett

Department of General Surgery, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong 510630, P.R. China.

Published: February 2020

AI Article Synopsis

  • Numerous studies show that microRNAs (miRs) play a crucial role in breast cancer (BC) progression, but the specific role of miR-3677, which is upregulated in BC, has not been explored until now.
  • The study found higher levels of miR-3677 in BC tissues and cell lines compared to non-cancerous tissues, and this overexpression led to increased cell proliferation, migration, and invasion of BC cells.
  • It identified TLE3 as a novel target gene for miR-3677; silencing TLE3 reduced the proliferation and migration of BC cells, suggesting that miR-3677 promotes BC progression by inhibiting TLE3, highlighting a potential new therapeutic target.

Article Abstract

Numerous studies have indicated an important function of microRNAs (miRs) in breast cancer (BC) progression, oncogenesis and metastasis. However, the function of miR-3677, which has been revealed to be upregulated in BC [The Cancer Genome Atlas (TCGA) data], has not been investigated to date. In the present study, miR-3677 was revealed to be upregulated in BC as determined using TCGA. miR-3677 was significantly upregulated in BC tissues and cell lines compared with those noted in adjacent non-cancerous tissues and primary normal breast cells (P<0.05). The overexpression of miR-3677 promoted the cell proliferation, migration and invasion of BC cells. Using bioinformatics algorithms and luciferase assays, a novel target gene for miR-3677, namely transducin-like enhancer of Split3 (TLE3), was identified. Silencing of TLE3 in miR-3677-transfected BC cells suppressed their proliferation and migration. An inverse correlation was observed between miR-3677 and TLE3 expression levels in human BC tissues. In conclusion, the present study demonstrated that miR-3677 promoted BC cell proliferation, migration and invasion by inhibiting TLE3 expression, which provided a novel mechanism and a promising therapeutic target for patients with BC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6960393PMC
http://dx.doi.org/10.3892/ol.2019.11241DOI Listing

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