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E6 and E7 of human papillomavirus type 18 and UVB irradiation corporately regulate interleukin‐6 and interleukin‐8 expressions in basal cell carcinoma
Author(s) -
Hsiao YuPing,
Yang JenHung,
Wu WenJun,
Lin MengHsuan,
Sheu GwoTarng
Publication year - 2013
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12223
Subject(s) - carcinogenesis , basal cell carcinoma , cell culture , cancer research , interleukin , microbiology and biotechnology , downregulation and upregulation , chemistry , interleukin 4 , skin cancer , biology , cytokine , immunology , cancer , basal cell , medicine , gene , biochemistry , genetics
The lack of a human papillomavirus ( HPV )‐infected skin cancer cell line has hampered the investigation of the interaction of UV and HPV in skin carcinogenesis. We identified a human basal cell carcinoma ( BCC ‐1/ KMC ) cell line integrated with E6 and E7 genes of high‐risk HPV type 18 and demonstrated that repression of E6 and E7 results in proliferation inhibition. Sublethal ultraviolet‐B ( UVB ) irradiation induced the expressions of interleukin‐6 (IL‐6) and interleukin‐8 (IL‐8), as well as viral E6 and E7 genes, in BCC‐1/KMC cells. When E6 and E7 expressions were inhibited, IL‐6/IL‐8 expressions were repressed. Furthermore, IL‐6/IL‐8 remained inducible by UVB irradiation when E6 and E7 were inhibited. These results indicated that IL‐6 and IL‐8 can be upregulated by viral E6 and E7 proteins without UVB irradiation. Moreover, chronic exposure to UVB upregulates IL‐6 and IL‐8 when E6/E7 is induced by UVB .