MiR-548d-3p/TP53BP2 axis regulates the proliferation andapoptosis of breast cancer cells.

Qiong Song,Yanling Ma,Nai Sun,Guishan Xia,Yanping Huo,Baolin Li,Jiangqiang Song,Longqiu Yang,Qimin Wang,Qiu Chen,Jieyu Ma

doi:10.1002/cam4.567

Abstract

Fast growth and hardly any apoptosis are important characteristics of breast cancer, which assure the spread via invasion and metastasis of breast cancer cells. Inhibition of fast proliferation and induction of apoptosis are critical way to cure this cancer. microRNAs (miRNAs) had been increasingly reported to be the critical regulator of tumorigenesis. In our study, we found that increasing copy number of miR-548d-2-3p is critically involved poor prognosis. We overexpressed miR-548d-3p in MDA-MB-231cells and found that the proliferation was promoted significantly, whereas the inhibition of miR-548d-3p repressed the proliferation of MDA-MB-231 cells and also induced the increase in apoptosis. Additionally, we found that miR-548d-3p downregulated the expression of TP53BP2 by directly targeting the 3'UTR. We also found that knockdown of TP53BP2 significantly resorted the proliferation and apoptosis regulated by miR-548d-3p inhibitor. Our study showed that miR-548d-3p/TP53BP2 pathway is critically involved in the proliferation and apoptosis of breast cancer cells and may be new therapeutic target of breast cancer cells.

Highlights

Breast cancer is a common cancer and causes many deaths of women
We detected the survival information and genomic profiles provided by the Cancer Genome Atlas (TCGA) about the copy-number value (CNV) of miR-548d-1-3p(chr8: 123348034-123348130 [−]) and miR-548d-2-3p(chr17: 67471489-67471585 [−])which have the same sequence but on the two different genomic DNA showed association with overall survival
DNA copy-number alterations frequently occur in breast cancer patient, which is defined as the key pathogenetic events

Summary

Introduction

Breast cancer is a common cancer and causes many deaths of women. Breast cancer cells have almost unlimited ability of survival with fast proliferation and less apoptosis [1]. The proliferation and apoptosis of breast cancer cells has been reported to be regulated by many core transcription factors or chromatin remodeling enzymes which form the circuitries [2,3,4,5]. TP53BP2 has been reported to be associated with the caner growth [6, 7]. It’s the critical factor and can cooperate with many other proteins to regulate the tumorigenesis of many kinds of cancer cells. TP53BP2 represses the squamous cell by regulating p63 [8]. TP53BP2 regulates p53-dependent apoptosis [9].

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Results

Conclusion