کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1930513 | 1050517 | 2011 | 6 صفحه PDF | دانلود رایگان |
Deficient DNA repair capacity is associated with genetic lesions accumulation and susceptibility to carcinogenesis. MicroRNAs (miRNAs) are small non-coding RNAs that regulate various cellular pathways including DNA repair. Here we hypothesized that the existence of HBV products may interfere with cellular nucleotide excision repair (NER) through microRNA-mediated gene regulation. We found that NER was impaired in HepG2.2.15 cells, a stable HBV-expressing cell line, compared with its parental cell line HepG2. Altered miRNA expression profile, in particular the significant upregulation of miR-192, was observed in HepG2.2.15 cells. Additionally, ERCC3 and ERCC4, two key factors implicated in NER, were identified as targets of miR-192 and over-expressing miR-192 significantly inhibited cellular NER. These results indicated that persistent HBV infection might trigger NER impairment in part through upregulation of miR-192, which suppressed the levels of ERCC3 and ERCC4. It provides new insight into the effect of chronic HBV infection on NER and genetic instability in cancer.
► Nucleotide excision repair is impaired in HepG2.2.15 cells.
► Altered miRNA expression including upregulation of miR-192 was observed in HepG2.2.15 cells.
► ERCC3 and ERCC4 are targets of miR-192.
► MiR-192 inhibits nucleotide excision repair.
Journal: Biochemical and Biophysical Research Communications - Volume 410, Issue 3, 8 July 2011, Pages 440–445