ArticleMolecular carcinogenesis2009
Enforced expression of PPP1R13L increases tumorigenesis and invasion through p53-dependent and p53-independent mechanisms.
Article in Molecular carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Function-driven design of a surrogate interleukin-2 receptor ligand.FEBS letters · 2026Article
- PPP1R13L drives cervical cancer progression by suppressing p63-mediated PTEN transcription.Cellular and molecular life sciences : CMLS · 2025Article
- Nucleotide excision repair gene polymorphisms and hepatoblastoma susceptibility in Eastern Chinese children: A five-center case-control study.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024Article
- Article
- Regulation of immunological tolerance by the p53-inhibitor iASPP.Cell death & disease · 2023Article
- Development of a ferroptosis-based model to predict prognosis, tumor microenvironment, and drug response for lung adenocarcinoma with weighted genes co-expression network analysis.Frontiers in pharmacology · 2022Article
- Development and clinical validation of a novel six-gene signature for accurately predicting the recurrence risk of patients with stage II/III colorectal cancer.Cancer cell international · 2021Article
- Long non-coding RNA AFAP1-AS1 plays an oncogenic role in promoting cell migration in non-small cell lung cancer.Cellular and molecular life sciences : CMLS · 2018Article
- Sertad1 antagonizes iASPP function by hindering its entrance into nuclei to interact with P53 in leukemic cells.BMC cancer · 2017Article
- Reactivating p53 functions by suppressing its novel inhibitor iASPP: a potential therapeutic opportunity in p53 wild-type tumors.Oncotarget · 2015Review
- An explorative analysis of ERCC1-19q13 copy number aberrations in a chemonaive stage III colorectal cancer cohort.BMC cancer · 2013Article
- Elevated expression of iASPP in head and neck squamous cell carcinoma and its clinical significance.Medical oncology (Northwood, London, England) · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
PPP1R13L was initially identified as a protein that binds to the NF-kappaB subunit p65/RelA and inhibits its transcriptional activity. It also binds p53 and inhibits its action. One set of experimental findings based on overexpression of PPP1R13L indicates that PPP1R13L blocks apoptosis. Another set of experiments, based on endogenous production of PPP1R13L, suggests that the protein may sometimes be pro-apoptotic. We have used primary mouse embryonic fibroblasts (MEFs), dually transformed by HRAS and adenovirus E1A and differing in their p53 status, to explore the effects of PPP1R13L overexpression, thus examining the ability of PPP1R13L to act as an oncoprotein. We found that overexpression of PPP1R13L strongly accelerated tumor formation by RAS/E1A. PPP1R13L overexpressing cells were depleted for both p53 and active p65/RelA and we found that both p53-dependent and -independent apoptosis pathways were modulated by PPP1R13L. Finally, studies with the proteasome inhibitor MG132 revealed that overexpression of PPP1R13L causes faster p53 degradation, a likely explanation for the depletion of p53. Taken together, our results show that increased levels of PPP1R13L can increase tumorigenesis and furthermore suggest that PPP1R13L can influence metastasis.
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