Figure 6.

TRPC7 knockout reduced the number of gene mutations in ultraviolet B (UVB)‐induced tumorigenesis. Whole‐exome sequencing was used to analyze the number of mutations in the dorsal skin of UVB‐exposed wild‐type (WT) and TRPC7 knockout mice (n = 3). Merged data from whole‐exome sequencing indicated (a) the number of mutations, (b) the contribution of each variant type, and (c) the number of mutations of each variant type. (d) A heat map illustrates the number of mutations from UVB‐induced tumorigenesis, (e) the mutations specific to the TRP gene family, and (f) the p53 family genes and p53‐dependent molecules. (g) Schematic representation of the role of TRPC7 as a potential tumor initiator gene in ultraviolet B (UVB)‐induced aging and cancer progression. UVB‐activated TRPC7 initiates UVB‐induced skin aging via intracellular Ca²⁺ elevation, resulting in oxidative stress, DNA damage response (DDR) activation, abnormal differentiation, and senescence inflammation response (SIR) activation; this pathology is repaired with the activation of p53 to maintain tissue homeostasis. When homeostasis is no longer maintained and the aging process is activated, carcinogens promote cancer progression. TRPC7 initiates tumorigenesis by causing genomic instability, thereby changing the activity of proto‐oncogenes and tumor suppressor genes. TRPC7 is also overexpressed in cancer progression, which may promote the cell cycle and cytoskeletal remodeling by increasing Ca²⁺ signaling