Ultraviolet (UV) radiation is a major environmental factor contributing to skin cancer development, particularly melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC). UV radiation is categorized into UVA (315–400 nm), UVB (280–320 nm), and UVC (100–280 nm) based on wavelength. UVA and UVB cause DNA damage through direct and indirect mechanisms, leading to mutations in genes like BRAF, NRAS, and TP53, which are critical in cancer development. UVA primarily causes indirect DNA damage via reactive oxygen species (ROS), while UVB causes direct DNA damage through cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). These DNA lesions are repaired by mechanisms such as nucleotide excision repair (NER), but mutations in genes like PTCH1 and SMO in the Hedgehog (Hh) pathway also contribute to BCC development. UV exposure increases the risk of melanoma through MC1R signaling and BRAF/NRAS mutations. UV radiation also promotes photoaging by increasing ROS, leading to MMP upregulation and skin damage. Melanoma diagnosis uses the ACBDE checklist and dermoscopy, while treatment includes BRAF/MEK inhibitors and immunotherapy. BCC is primarily caused by Hh pathway mutations, with PTCH1 and SMO mutations playing key roles. SCC is linked to UV exposure, HPV, and TP53 mutations. UV protection, including sunscreen use, is crucial in reducing cancer risk. Advances in AI and targeted therapies are improving diagnosis and treatment outcomes for skin cancers.Ultraviolet (UV) radiation is a major environmental factor contributing to skin cancer development, particularly melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC). UV radiation is categorized into UVA (315–400 nm), UVB (280–320 nm), and UVC (100–280 nm) based on wavelength. UVA and UVB cause DNA damage through direct and indirect mechanisms, leading to mutations in genes like BRAF, NRAS, and TP53, which are critical in cancer development. UVA primarily causes indirect DNA damage via reactive oxygen species (ROS), while UVB causes direct DNA damage through cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). These DNA lesions are repaired by mechanisms such as nucleotide excision repair (NER), but mutations in genes like PTCH1 and SMO in the Hedgehog (Hh) pathway also contribute to BCC development. UV exposure increases the risk of melanoma through MC1R signaling and BRAF/NRAS mutations. UV radiation also promotes photoaging by increasing ROS, leading to MMP upregulation and skin damage. Melanoma diagnosis uses the ACBDE checklist and dermoscopy, while treatment includes BRAF/MEK inhibitors and immunotherapy. BCC is primarily caused by Hh pathway mutations, with PTCH1 and SMO mutations playing key roles. SCC is linked to UV exposure, HPV, and TP53 mutations. UV protection, including sunscreen use, is crucial in reducing cancer risk. Advances in AI and targeted therapies are improving diagnosis and treatment outcomes for skin cancers.