Narrative review: mechanism of ultraviolet radiation-induced basal cell carcinoma

Wanlin Fan, Alexander C. Rokohl, Yongwei Guo, Hong Chen, Tao Gao, Vinodh Kakkassery, Ludwig M. Heindl*

*Corresponding author for this work
1 Citation (Scopus)


Background and Objective: Basal cell carcinoma (BCC) is the most widespread malignant skin cancer and also the most common cancer in adults. Although its mortality rate is low, its incidence is increasing, especially in Caucasians. Among many risk factors, ultraviolet radiation (UVR) is the essential factor in forming BCC. However, the molecular mechanisms leading to transformation are not fully understood. This review provides a comprehensive description of the interaction of UVR and genetic features in the pathogenesis of BCC, and specifically, current advances in molecular therapy based on these mechanisms are introduced. Methods: A literature search was performed in the PubMed database using the search algorithms [(basal cell carcinoma) OR (BCC)] AND [(gene mutation) AND (ultraviolet radiation) AND (carcinogenesis)] to identify relevant publications until April 1, 2020. The database search was not restricted to any language, and relevant references were searched from the identified articles. Key Content and Findings: This review summarizes the potential mechanisms underlying BCC development due to UVR. UVB can be directly absorbed by DNA and induce skin cancer through intracellular signaling leading to DNA damage and altered gene expression. UVA radiation generates reactive oxygen species (ROS), which causes skin cancer through secondary damage to DNA and usually requires long-term cumulative exposure. Cells can repair damaged DNA, but DNA repair may be faulty due to genetic or environmental factors. As a result, mutations in proto-oncogenes and suppressor genes may occur, leading to tumor formation. Various immune responses of the body are usually reduced after UVR. UVR damages DNA, and its repair system alters the immune system and leads to progressive genetic alterations and tumor formation, genetic alterations, and tumor formation. Based on these advances in molecular mechanisms, targeted therapies such as smoothened (SMO) inhibitors (vismodegib and sonidegib), and immunotherapy such as pembrolizumab [anti-programmed cell death-1 (PD-1)] have been developed. Further future studies on the molecular genetics of UVR in the development of BCC may facilitate new targeted therapies and chemoprevention, thus improving treatment efficacy and prevention. Conclusions: This review highlights UVR damages DNA and its repair mechanisms, suppression the immune system, causes progressive gene mutations, and ultimately leads to tumor formation. Further studies on the molecular mechanisms associated with BCC will help raising public awareness of UV protection and explore new targeted therapeutic and chemopreventive means.

Original languageEnglish
Article number9
JournalFrontiers of Oral and Maxillofacial Medicine
Publication statusPublished - 10.03.2023

Research Areas and Centers

  • Research Area: Luebeck Integrated Oncology Network (LION)
  • Centers: University Cancer Center Schleswig-Holstein (UCCSH)

DFG Research Classification Scheme

  • 205-14 Haematology, Oncology
  • 206-11 Ophthalmology

Cite this