Journal
VIRUS GENES
Volume 58, Issue 2, Pages 88-97Publisher
SPRINGER
DOI: 10.1007/s11262-022-01887-8
Keywords
ATF3; HPV18; HeLa cells; p53; E6
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Funding
- Shiraz University of Medical Sciences, Shiraz, Iran [94-01-10-11107]
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Overexpression of ATF3 increases apoptosis in HPV-18-infected HeLa cells, but has no significant effect on the levels of p53 and E6. ATF3 acts as a tumor suppressor through a p53-independent pathway in HPV18-related cervical cancer.
Activating transcription factor 3 (ATF3) is the first p53 stability regulator that interferes with the ubiquitination of p53. However, the E6 oncoprotein of high-risk human papillomaviruses (HPVs) binds to and induces proteasome-dependent degradation of the host p53 protein. Herein, we investigate the effects of ATF3 overexpression on cell cycle progression and apoptosis in HPV-18-infected HeLa cells, and further examine whether ATF3 could alter the apoptosis level of HeLa cells through the inhibition of E6-mediated p53 degradation. Cytological function of HeLa cells prior and subsequent to the overexpression of ATF3 was assessed using cell cycle and annexin V/PI flow cytometry analysis. Western blotting assays revealed no significant effect of ATF3 on the levels of p53 and E6 in HeLa cells. However, annexin V staining demonstrated increases in apoptosis. ATF3 acts as a tumor suppressor factor in HPV18-related cervical cancer which mediates apoptotic functions through a p53-independent pathway.
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