Downregulation of miR-142-3p Contributes to Breast Cancer Oncogenesis

Author Info

Gangping WANG Huifang Shi Jingjing Li Lei Chen Shuguang Yang Ying Zhao Zuofeng Zhang

Corresponding Author

Gangping WANG
Department of Central Laboratory & Department of Pathology, Rizhao People’s Hospital, Affiliated to Jining Medical University, Rizhao 276826, China

A B S T R A C T

Breast cancer is one of the commonly-encountered malignant tumors, and its morbidity is on the rise year by year. A better understanding of the molecular mechanisms of breast cancer is important. This can improve the prevention, diagnosis, and treatment.The miR-142‐3p has been shown to inhibit carcinogenesis by regulating various cellular processes, including cell cycle progression, cell migration, apoptosis, and invasion. We surgically recruited 96 breast cancer patients and the breast cancer samples, each with matched adjacent normal breast tissue were obtained, MDA-MB-231 and MCF-7 cells were cultured for experiments in vitro and measured the expression of miR‐142‐3p via quantitative real‐time polymerase chain reaction (qRT‐PCR). Cell viability, apoptosis, migration, and invasion were determined by MTT, flow cytometry, and trans-well assays. The expression of miR-142-3p was down-regulated in both cancer cell lines and cancer specimens. The reduced expression of miR-142‐3p was associated with tumor size, lymph node metastasis, and tumor-node-metastasis (TNM) stage of patients (p<0.05). However, there was no significant correlation between miR‐142‐3p expression in tumor tissues with age at diagnosis (p>0.05). Overexpression of miR-142-3p repressed cell viability, migration, and invasion, while it induced apoptosis, whereas its depletion promoted it. The results suggest miR‐142‐3p acts as a tumor suppressor and can act as a novel target for the treatment of breast cancer. Thus, restoration of miR‐142‐3p expression, for example, via miRNA replacement therapy, may represent an effective strategy for the treatment of breast cancer patients

Article Info

Article Type

Research Article

Publication history

Received: Thu 21, Nov 2019
Accepted: Thu 05, Dec 2019
Published: Mon 16, Dec 2019

Copyright

© 2023 Gangping WANG. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.
DOI: 10.31487/j.COR.2019.6.11