High intensity interval training as a therapy: Mitophagy restoration in breast cancer

• Published in: Archives of biochemistry and biophysics 2024-12, Vol.762, p.110213, Article 110213
• Main Authors: Khoramipour, Kayvan, Soltany, Afsaneh, Khosravi, Pouria, Rezaei, Maryam Hossein, Madadizadeh, Elham, García-Chico, Celia, Maroto-Izquierdo, Sergio, Khoramipour, Karen
• Format: Article
• Language: English
• Subjects: AMP-Activated Protein Kinases - metabolism; Animals; Autophagy-Related Protein-1 Homolog - metabolism; Breast cancer; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Breast Neoplasms - therapy; Cell Line, Tumor; Exercise; Female; High-Intensity Interval Training; Mammary Neoplasms, Experimental - metabolism; Mammary Neoplasms, Experimental - pathology; Mammary Neoplasms, Experimental - therapy; Mice; Mice, Inbred BALB C; Microtubule-Associated Proteins - metabolism; Mitophagy; Physical Conditioning, Animal; Protein Kinases - metabolism; Sirtuin 1 - metabolism; Tumor volume; Ubiquitin-Protein Ligases - metabolism
• ISSN: 0003-9861; 1096-0384; 1096-0384
• DOI: 10.1016/j.abb.2024.110213

Recent studies have highlighted the role of mitophagy in tumorigenesis. This study aimed to investigate the effects of high-intensity interval training (HIIT) on mitophagy in tumor tissues of mice with breast cancer. Twenty-eight female BALB/c mice were randomly assigned to four groups: Healthy Control (CO), Cancer (CA), Exercise (EX), and Cancer + Exercise (CA + EX). Mammary tumors were induced in the CA and CA + EX groups via 4T1 cell injections. Upon confirmation of tumor formation, the EX and CA + EX groups underwent 8 weeks (40 sessions) of HIIT, comprising 4–10 intervals of running at 80–100 % of maximum speed. The expression levels of mitophagy-related proteins, including parkin, PTEN-induced putative kinase 1 (PINK1), NIP3-like protein X (NIX), BCL2 interacting protein-3 (BINP3), microtubule-associated protein light chain 3-I (LC3-I), microtubule-associated protein light chain 3-II (LC3-II), AMP-activated protein kinase (AMPK), Unc-51 like autophagy activating kinase-1 (ULK1), and sirtuin-1 (SIRT1), were measured in breast and tumor tissues. Tumor volume relative to body weight was assessed weekly during the eight-week HIIT intervention. Protein expression of parkin, PINK1, NIX, BINP3, LC3-II, LC3-I, AMPK, ULK1, and SIRT1 was reduced in the breast tissue of the CA group, while HIIT restored expression levels across all measured variables (P