Bai J, Chen WB, Zhang XY, Kang XN, Jin LJ, Zhang H, Wang ZY. HIF-2α regulates CD44 to promote cancer stem cell activation in triple-negative breast cancer via PI3K/AKT/mTOR signaling. World J Stem Cells 2020; 12(1): 87-99 [PMID: 32110277 DOI: 10.4252/wjsc.v12.i1.87]
Corresponding Author of This Article
Zun-Yi Wang, MD, Doctor, Department of Third Surgical Oncology, Cangzhou Central Hospital, No. 16, West Xinhua Road, Cangzhou 061001, Hebei Province, China. czwzy99@163.com
Research Domain of This Article
Oncology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Stem Cells. Jan 26, 2020; 12(1): 87-99 Published online Jan 26, 2020. doi: 10.4252/wjsc.v12.i1.87
HIF-2α regulates CD44 to promote cancer stem cell activation in triple-negative breast cancer via PI3K/AKT/mTOR signaling
Jie Bai, Wei-Bin Chen, Xiao-Yu Zhang, Xiao-Ning Kang, Li-Jun Jin, Hui Zhang, Zun-Yi Wang
Jie Bai, Xiao-Yu Zhang, Li-Jun Jin, Zun-Yi Wang, Thyroid and Breast Deptartment III, Cangzhou Central Hospital, Cangzhou 061001, Hebei Province, China
Wei-Bin Chen, Department of Radiology, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, Hebei Province, China
Xiao-Ning Kang, Department of Second Ultrasound, Cangzhou Central Hospital, Cangzhou 061001, Hebei Province, China
Author contributions: Bai J and Wang ZY conceived and designed the study; Bai J, Chen WB, and Zhang XY performed the experiments; Zhang XY and Kang XN acquired the patients’ data; Bai J, Kang XN, Jin LJ, and Zhang H analyzed the data and drafted the report; Wang ZY supervised the study; all authors reviewed and revised the manuscript critically and approved the final version to be published.
Institutional review board statement: The study was approved by the Ethics Committee of Cangzhou Central Hospital.
Conflict-of-interest statement: The authors report no conflicts of interest in this work.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Zun-Yi Wang, MD, Doctor, Department of Third Surgical Oncology, Cangzhou Central Hospital, No. 16, West Xinhua Road, Cangzhou 061001, Hebei Province, China. czwzy99@163.com
Received: June 15, 2019 Peer-review started: June 18, 2019 First decision: July 31, 2019 Revised: August 12, 2019 Accepted: October 14, 2019 Article in press: October 14, 2019 Published online: January 26, 2020
Core Tip
Core tip: Cancer stem cells (CSCs) play an important role in tumor formation, growth, invasion, metastasis, and recurrence. Hypoxia can promote the differentiation of various tumor cells, enable cells to acquire stem cell characteristics, and enhance tumor cell invasion and tumorigenicity. In the long-term exposure of tumors to hypoxia, the major regulatory factor is hypoxia-inducible factor-2α (HIF-2α), which can promote the malignant biological behavior of tumors by activating its downstream target genes. Studies have shown that the effect of HIF-2α on tumor cells may be related to CD44, a marker for breast CSCs. In this study, breast cancer cell line MCF-7 and basal breast cancer cell line MDA-MB-231 were utilized to investigate the relationship between HIF-2α and CD44 gene expression and the regulatory effect of HIF-2α on CD44.
