The Effect of Eight Weeks of Aerobic Exercise on Gene Expression of Cytochrome C, Caspase 9 and Tumor Volume in Mice with Breast Cancer
محورهای موضوعی :
Report of Health Care
Mohammad Mahdi Rafiei
1
,
Abbasali Gaeini
2
,
Mohamad Reza Kordi
3
,
Reza Nuri
4
1 - Department of Exercise Physiology, University of Tehran, Kish International Campus, Kish, Iran
2 - Department of Exercise Physiology, Tehran University, Tehran, Iran
3 - Department of Exercise Physiology, Tehran University, Tehran, Iran
4 - Department of Exercise Physiology, University of Tehran, Kish International Campus, Kish, Iran
تاریخ دریافت : 1397/07/06
تاریخ پذیرش : 1397/07/06
تاریخ انتشار : 1397/07/09
کلید واژه:
Cancer,
Exercise,
Apoptosis,
چکیده مقاله :
Introduction: Breast cancer is a malignant tumor characterized by uncontrolled proliferation of cancerous cells by exposure to the risk of death. Therefore, this study aimed to investigate the effect of eight weeks of aerobic exercise on cytochrome C, caspase 9 and tumor volume in mice with breast cancer. Methods: In this experimental study, 20 female balb/c mice (age: five to six weeks) were injected with MC4-L2 cancerous cells. They were then randomly assigned to two groups of 10 mice including experimental and control groups. Experimental group performed exercise for eight weeks (55-70% of the aerobic capacity of the mice). 48 hours after the last training session, the mice were sacrificed and their tumors tissue samples were removed and stored at -70 ° C and the level of factor expression of cytochrome C and caspase-9 of tumor tissue was measured by Real Time-PCR. Data were analyzed by SPSS21 using independent sample t- test (p≤ 0.05). Results: There was a significant difference between the two groups of control and aerobic exercise in the cytochrome C (P = 0.001) and caspase 9 (P = 0.039), and the levels were higher in the exercise group than in the control group. Also, regarding tumor volume index, tumor volume in the exercise group was significantly less than that in the control group (P = 0.001). Conclusion: In general, the results of this study confirm the positive role of eight weeks of aerobic exercise by stimulating upstream factors affecting the process of cancerous cell apoptosis.
منابع و مأخذ:
Munshi A, Pai RH, Phurailatpam R, Budrukkar A, Jalali R, Sarin R, et al. Do all patients of breast carcinoma need 3-dimensional CT-based planning? A dosimetric study comparing different breast sizes. Med Dosim. 2009; 34 (2): 140- 144.
Mooren F, Völker K. Molecular and cellular exercise physiology. Human Kinetics; 2004.
Phanuef Sh, Leeuwenburgh Ch. Apoptosis and exercise. Med Sci Sports Exerc. 2001; 33 (3): 393- 396.
Degterev A, Boyce M, Yuan J. A decade of caspases. Oncogene. 2003; 22 (53): 8543- 8567.
Devarajan E, Sahin A, Chen J. Down-regulation of caspase 3 in breast cancer: a possible mechanism for chemoresistance. Oncogene. 2002; 21 (57): 8843- 8851.
Johnsson A, Johnsson A, Johansson K. Physical activity during and after adjuvant chemotherapy in patients with breast cancer. Physiol J. 2013; 99 (3): 221- 227.
Douglas R, Abdalla Eddie FC, Murta Marcia A. The influence of physical activity on the profile of immune response cells and cytokine synthesis in mice with experimental breast tumors induced by dimethylbenzanthracene. Eur J Cancer Prev. 2013; 22 (3): 251- 258.
Melinda L, Irwin EJA, Anne McT, Leslie B, Frank DG, Richard NB, et al. Physical activity, body mass index, and mammographic density in postmenopausal breast cancer survivors. J Clin Oncol. 2007; 25 (9): 1061- 1066.
Amani Shalamzari S, Agha-Alinejad H, Alizadeh SH, et al. The effect of exercise training on the level of tissue IL-6 and vascular endothelial growth factor in breast cancer bearing mice. Iran J Basic Med Sci. 2014; 17: 231- 236.
Biral D, J-Puka A, Betto R. Expression of Bcl- 2 family proteins in recovering and regenerating muscles. Basic Appl Myol. 2002; 12 (1): 43- 46.
Fernandes Silva MM, Oliveira Carvalho V, Veiga Guimarães G, Bacal F, Alcides B. Physical exercise and microRNAs: new frontiers in heart failure. Bras Cardiol. 2012; 98 (5): 459- 466.
Kadi F, Schjerling P, Andersen LL, Charifi N, Madsen JL, Christensen LR, et al. The effects of heavy resistance training and detraining on satcllite cells – in human skeletal muscles. J Physiol. 2004; 558 (3): 1005- 1012.
Jones LW, Viglianti BL, Tashjian JA, Kothadia SM, Keir ST, Freedland SJ, et al. Effect of aerobic exercise on tumor physiology in an animal model of human breast cancer. J Appl Physiol. 2010; 108 (4): 1021.
Hoydal MA, Wisløff U, Kemi OJ, Ellingsen O. Running speed and maximal oxygen uptake in rats and mice: practical implications for exercise training. Eur J Cardiovasc Prev Rehabil. 2007; 14 (6): 753- 760.
Parco M, Bryner RW, Martyn LK, Always SE. Apoptotic adaptations from exercise training in skeletal and cardiac muscles. FASEB J. 2004; 18 (10): 1150- 1152.
Amini A, Gaiini AA, Choobineg S, Kordi MR, Alizadeh Sh. The effect of eight weeks of aerobic exercise on the gene expression of Bcl-2, miR-15 and Bcl-2 protein of tumor tissue in mice with breast cancer. Sports Physiol. 2016; 32 (1): 100- 108.
Scott L. The role of mitochondria in the mammalian antiviral defense system. Mitochondrion. 2010; 10 (4): 316- 320.
Bayir H, Kagan VE. Bench-to-bedside review: Mitochondrial injury, oxidative stress and apoptosis- there is nothing more practical than a good theory. Critical Care. 2008; 12 (1): 1- 11.
Soberanes S, Panduri V, Mutlu GM, Ghio A, Scott Bundinger GR, Kamp DW. P53 mediates particulate matter induced alveolar epithelial cell mitochondriaregulated apoptosis. Am J Respir Crit Care Med. 2006; 174: 1229- 1238.
Pfeffer CM, Singh ATK. Apoptosis: A Target for Anticancer Therapy. Int J Mol Sci. 2018; 19 (2): E448.
Connolly PF, Fearnhead HO. Viral hijacking of host caspases: an emerging category of pathogen-host interactions. Cell Death Differ. 2017; 24 (8): 1401- 1410.
Dawar S, Lim Y, Puccini J, White M, Thomas P, Bouchier- Hayes L, et al. Caspase-2-mediated cell death is required for deleting aneuploid cells. Oncogene. 2017; 36 (19): 27040- 2714.
Crockford A, Zalmas LP, Grönroos E, Dewhurst SM, McGranahan N, Cuomo ME, et al. Cyclin D mediates tolerance of genome-doubling in cancers with functional p53. Ann Oncol. 2017; 28 (1): 149- 156.