Affiliations 

  • 1 Department of Thyroid and Breast Surgery, Jingmen City People's Hospital, Jingchu University of Technology, Jingmen, Hubei, P.R. China
  • 2 Department of Oncology, Jingmen City People's Hospital, Jingmen, Hubei, P.R. China
  • 3 Department of General Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, P.R. China
  • 4 Forensic Appraisal Center of Jingmen Public Security Jingmen, Hubei, P.R. China
Protein Pept Lett, 2023;30(12):992-1000.
PMID: 38013437 DOI: 10.2174/0109298665245603231106050224

Abstract

OBJECTIVES: We aim to investigate the regulatory mechanisms of miR-455-5p/SOCS3 pathway that underlie the proliferation, migration, and invasion of triple-negative breast cancer (TNBC) cells.

METHODS: Reverse transcription-quantitative PCR (RT-qPCR) was used to detect miR-455-5p expression in breast cancer tissues and cell lines. CCK8 and Transwell assays were conducted to assess the effects of miR-455-5p on breast cancer line proliferation, migration, and invasion. SOCS3 expression level in breast cancer tissues and cell lines was determined by qPCR and western blotting. The targeting relationship between miR-455-5p and SOCS3 was determined by dual luciferase reporter gene assay in different breast cancer cell lines. Finally, the upstream and downstream regulatory association between miR-455-5p and SOCS3 was confirmed in breast cancer cells by CCK8, western blot, and Transwell assays.

RESULTS: MiR-455-5p expression was up-regulated in breast cancer tissues; miR-455-5p regulates TNBC proliferation, migration, and invasion of TNBC. SOCS3 was the direct target of miR-455-5p and was down-regulated in breast cancer. Interference with SOCS3 reversed the inhibitory effect of the miR-455-5p inhibitor on breast cancer cells' malignant potential.

CONCLUSION: MiR-455-5p promotes breast cancer progression by targeting the SOCS3 pathway and may be a potential therapeutic target for breast cancer.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.