Department of Microbiology and Cell Biology, Indian Institute of Science, Bengaluru, India.
Department of Biochemistry, Indian Institute of Science, Bengaluru, India.
Sci Rep. 2018 Apr 4;8(1):5599. doi: 10.1038/s41598-018-23669-9.
Cardiomyopathy is one of the characteristic features of cancer. In this study, we establish a suitable model to study breast cancer-induced cardiomyopathy in mice. We used Ehrlich Ascites Carcinoma cells to induce subcutaneous tumor in 129/SvJ mice and studied its effect on heart function. In Ehrlich Ascites Carcinoma bearing mice, we found significant reduction in left ventricle wall thickness, ejection fraction, and fractional shortening increase in left ventricle internal diameter. We found higher muscle atrophy, degeneration, fibrosis, expression of cell-adhesion molecules and cell death in tumor-bearing mice hearts. As observed in cancer patients, we found that mTOR, a key signalling molecule responsible for maintaining cell growth and autophagy was suppressed in this model. Tumor bearing mice hearts show increased expression and nuclear localization of TFEB and FoxO3a transcription factors, which are involved in the upregulation of muscle atrophy genes, lysosomal biogenesis genes and autophagy genes. We propose that Ehrlich Ascites Carcinoma induced tumor can be used as a model to identify potential therapeutic targets for the treatment of heart failure in patients suffering from cancer-induced cardiomyopathy. This model can also be used to test the adverse consequences of cancer chemotherapy in heart.
心肌病是癌症的特征之一。在本研究中,我们建立了一个合适的模型来研究小鼠中由乳腺癌引起的心肌病。我们使用艾氏腹水癌细胞在 129/SvJ 小鼠中诱导皮下肿瘤,并研究其对心脏功能的影响。在患有艾氏腹水癌的小鼠中,我们发现左心室壁厚度、射血分数和左心室内径缩短分数明显降低。我们发现肿瘤小鼠心脏中肌肉萎缩、变性、纤维化、细胞黏附分子表达和细胞死亡增加。与癌症患者观察到的情况一样,我们发现,mTOR(一种负责维持细胞生长和自噬的关键信号分子)在该模型中受到抑制。肿瘤小鼠心脏中 TFEB 和 FoxO3a 转录因子的表达和核定位增加,这涉及肌肉萎缩基因、溶酶体生物发生基因和自噬基因的上调。我们提出,艾氏腹水癌诱导的肿瘤可作为一种模型,用于确定治疗癌症引起的心肌病患者心力衰竭的潜在治疗靶点。该模型还可用于测试心脏化疗的不良后果。