Open Access

ARTICLE

UBE2T mediates the stemness properties of breast cancer cells through the mTOR signaling pathway

by JIAWEI YIN¹, YONGSHENG WANG^2,3, GUANGWEI WEI⁴, MINGXIN WEN^3,*

1 Department of Traumatology, The Second Hospital of Shandong University, Jinan, 250033, China
2 Department of Pathology, Weifang People’s Hospital, Weifang, 261000, China
3 Department of Human Anatomy, Shandong University School of Medicine, Jinan, 250012, China
4 Department of Cell Biology and Key Laboratory of Experimental Teratology, Shandong University School of Medicine, Jinan, 250012, China

* Corresponding Author: MINGXIN WEN. Email:

(This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)

BIOCELL 2024, 48(6), 959-970. https://doi.org/10.32604/biocell.2024.049349

Received 04 January 2024; Accepted 03 April 2024; Issue published 10 June 2024

Abstract

Objectives: This study aimed to reveal the role and possible mechanism of the ubiquitin-conjugating enzyme 2T (UBE2T) in the biological activities of breast cancer stem cells (BCSCs). Methods: The specific protein and gene expression were quantified by Western blotting and quantitative real-time polymerase chain reaction, the proportion of BCSCs was examined by flow cytometry, and the self-renewal and proliferation of BCSCs were verified by serial sphere formation and soft agar. Results: Increasing expression of UBE2T was drastically found in breast cancer than that in adjacent tissues. Furthermore, UBE2T overexpression significantly increased the proportion of BCSCs in breast cancer cells and promoted their self-renewal and proliferation. Silent UBE2T exhibited the opposite functions. UBE2T increased the levels of the mammalian target of rapamycin and the phosphorylated mammalian target of rapamycin. Mammalian target of rapamycin (mTOR) inhibitor rapamycin inhibited the function of UBE2T in BCSCs. Conclusion: UBE2T plays a role in BCSCs through mTOR pathway and may suggest a novel therapeutic strategy for breast cancer.

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Keywords

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