Mitochondrial depletion or CCCP induced the expression of both insulin and IGF-1 receptor (IGF-1R) but selectively activated IGF-1R in a Cn-dependent manner in the myoblast cell line C2C12, which is responsible for Akt activation leading to enhanced glucose uptake and tumor invasion.(89) Intriguingly, this induction of IGF-1R by mitochondrial stress has been observed in many cancer cell lines, including A549, H9C2 cardiomyocytes, and NIH3T3 cells. This evidence concerns the gene IGF1R and neoplasm.