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Transcriptional repression of smooth‐muscle α‐actin gene associated with human papillomavirus type 16 E7 expression
Author(s) -
Nishida Makoto,
Miyamoto Shingo,
Kato Hidenori,
Miwa Takeshi,
Imamura Toshiro,
Miwa Katsuhiro,
Yasumoto Shigeru,
Barrett J. Carl,
Wake Norio
Publication year - 1995
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940130305
Subject(s) - chloramphenicol acetyltransferase , biology , psychological repression , microbiology and biotechnology , reporter gene , actin , cytoskeleton , gene expression , acetyltransferase , regulation of gene expression , transfection , gene , cell , genetics , acetylation
To explore the role of the E7 viral oncogene from human papillomavirus type 16 (HPV16) in the regulation of cytoskeletal organization, we investigated alterations in particular cytoskeletal components in rat embryonal fibroblasts and three transformants of rat embryonal fibroblast cells produced by transfertions with HPV16 E7 alone (TF1), HPV16 E7 plus adenovirus type 5 E1B (TF3), and HPV16 E7 plus activated Ha‐ ras (TF4). Marked reductions in smooth‐muscle (SM) a‐actin content and disrupted organization of stress fibers detected by anti—SM α‐actin antibody were evident in all the transformants. These cytoskeletal manifestations were associated with a significant reduction in the mRNAs in these cells. Transcriptional repression by the E7 gene was observed after transient transfection of a chloramphenicol acetyltransferase reporter gene with SM α‐actin gene promoter. Nucleotides —123 to —39 of the SM α‐actin gene promoter were required for the HPV16 E7 transcriptional repression as shown by the chloramphenicol acetyltransferase assay. The downregulation of this actin isoform mediated by the E7 oncoprotein may play an important role in cell transformation by HPV16. © 1995 Wiley‐Liss, Inc.