ArticleOncogene2014
Star-PAP controls HPV E6 regulation of p53 and sensitizes cells to VP-16.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Rethinking residual p53 function in HPV-positive cervical cancer cells.Journal of virology · 2026Article
- The poly(A) polymerase Star-PAP is regulated by stably associated phosphoinositide messengers.The Journal of biological chemistry · 2025Article
- Star-PAP regulates tumor protein D52 through modulating miR-449a/34a in breast cancer.Biology open · 2019Article
- Nuclear Phosphatidylinositol-Phosphate Type I Kinase α-Coupled Star-PAP Polyadenylation Regulates Cell Invasion.Molecular and cellular biology · 2018Article
- Nuclear phosphoinositide regulation of chromatin.Journal of cellular physiology · 2018Review
- 3-(2-Chloropropyl amide)-4-methoxy-N-phenylbenzamide inhibits expression of HPV oncogenes in human cervical cancer cell.Virology journal · 2017Article
- Star-PAP, a poly(A) polymerase, functions as a tumor suppressor in an orthotopic human breast cancer model.Cell death & disease · 2017Article
- IQGAP1 is a phosphoinositide effector and kinase scaffold.Advances in biological regulation · 2016Review
- Cell-based screen for altered nuclear phenotypes reveals senescence progression in polyploid cells after Aurora kinase B inhibition.Molecular biology of the cell · 2015Article
- PIP kinases define PI4,5P₂signaling specificity by association with effectors.Biochimica et biophysica acta · 2015Review
- BAG3 down-modulation sensitizes HPV18(+) HeLa cells to PEITC-induced apoptosis and restores p53.Cancer letters · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cervical cancer is the most common genital malignancy and the high-risk human papillomaviruses (HPV type 16, 18 and 31, and so on) are major agents for its cause. A key switch for the onset of cervical cancers by HPVs is the cellular degradation of the tumor-suppressor p53 that is mediated by the HPV-generated E6 protein. E6 forms a complex with the E3 ubiquitin-ligase E6-associated protein (E6AP) leading to p53 degradation. The components that control E6 expression and the mechanisms for regulation of the expression in host cells remain undefined. Here we show that the nuclear noncanonical poly(A) polymerase (PAP) speckle targeted PIPKIα regulated PAP (Star-PAP) controls E6 mRNA polyadenylation and expression and modulates wild-type p53 levels as well as cell cycle profile in high-risk HPV-positive cells. In the absence of Star-PAP, treatment of cells with the chemotherapeutic drug VP-16 dramatically reduced E6 and increased p53 levels. This diminished both cell proliferation and anchorage-independent growth required for cancer progression, indicating a synergism between VP-16 treatment and the loss of Star-PAP. This identifies Star-PAP as a potential drug target for the treatment of HPV-positive cancer cells. These data provide a mechanistic basis for increasing the sensitivity and efficiency of chemotherapy in the treatment of cancers that have low levels of wild-type p53.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.