Research Paper Volume 11, Issue 22 pp 10203—10219
Mitochondrial fission regulator 2 (MTFR2) promotes growth, migration, invasion and tumour progression in breast cancer cells
- 1 Department of Breast and Thyroid Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Basie, Guangxi, China
- 2 Department of Breast and Thyroid Surgery, Eastern Hospital of the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
- 3 Department of Breast and Thyroid Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Ji’nan, Shandong, China
- 4 Department of Breast and Thyroid Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
- 5 Department of Stomatology, Affiliated Hospital of Youjiang Medical University for Nationalities, Basie, Guangxi, China
- 6 Department of Oncology, Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China
- 7 Department of Breast and Thyroid Surgery, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
- 8 Division of Thyroid and Parathyroid Endocrine Surgery, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA
Received: August 22, 2019 Accepted: October 29, 2019 Published: November 18, 2019
https://doi.org/10.18632/aging.102442How to Cite
Copyright © 2019 Lu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Introduction: Mitochondrial fission regulator 2 (MTFR2) belongs to the MTFR family, and 2 isoforms of MTFR2 are produced by alternative splicing. The role of MTFR2 in breast cancer (BC) remains unknown.
Results: MTFR2 was upregulated in BC tissues and was strongly associated with tumor characteristics. Moreover, Kaplan-Meier and Cox proportional hazards analyses indicated that high MTFR2 expression was related to poor overall survival. In addition, the capacity for migration and invasion decreased in two BC cell lines after knockdown of MTFR2. The epithelial-mesenchymal transition pathway was inhibited in MTFR2-silenced cells. MTFR2 can switch glucose metabolism from OXPHS to glycolysis in a HIF1α- and HIF2α-dependent manner.
Conclusion: Taken together, our results indicate that increased expression of MTFR2 is associated with tumour progression in breast cancer cells through switching glucose metabolism from OXPHS to glycolysis in a HIF1α- and HIF2α-dependent manner.
Materials and methods: We obtained data from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) to analyse MTFR2 expression in BC. The prognostic value of MTFR2 expression was assessed using the Kaplan-Meier method. The biological influence of MTFR2 on BC cell lines was studied using proliferation, Transwell migration, invasion and mitochondrial function assays.