ArticleCell death & disease2012
PP2A inactivation is a crucial step in triggering apoptin-induced tumor-selective cell killing.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- MicroRNAs as the critical regulators of autophagy-mediated cisplatin response in tumor cells.Cancer cell international · 2023Review
- YTHDF2 exerts tumor-suppressor roles in gastric cancer via up-regulating PPP2CA independently of mBiological procedures online · 2023Article
- Genetic deletion of Nox4 enhances cancerogen-induced formation of solid tumors.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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- The natural anticancer agent cantharidin alters GPI-anchored protein sorting by targeting Cdc1-mediated remodeling in endoplasmic reticulum.The Journal of biological chemistry · 2019Article
- KIAA1199 promotes metastasis of colorectal cancer cells via microtubule destabilization regulated by a PP2A/stathmin pathway.Oncogene · 2019Article
- Does BCA3 Play a Role in the HIV-1 Replication Cycle?Viruses · 2018Article
- Upregulation of AKIP1 contributes to metastasis and progression and predicts poor prognosis of patients with colorectal cancer.OncoTargets and therapy · 2018Article
- MiR-320 regulates cardiomyocyte apoptosis induced by ischemia-reperfusion injury by targeting AKIP1.Cellular & molecular biology letters · 2018Article
- Proteomic View of the Crosstalk betweenFrontiers in microbiology · 2017Article
- miR-222 attenuates cisplatin-induced cell death by targeting the PPP2R2A/Akt/mTOR Axis in bladder cancer cells.Journal of cellular and molecular medicine · 2016Article
- Overexpression of AKIP1 predicts poor prognosis of patients with breast carcinoma and promotes cancer metastasis through Akt/GSK-3β/Snail pathway.American journal of translational research · 2016Article
- The chimeric multi-domain proteins mediating specific DNA transfer for hepatocellular carcinoma treatment.Cancer cell international · 2016Article
- PP2A: The Wolf in Sheep's Clothing?Cancers · 2015Review
- Viral genes as oncolytic agents for cancer therapy.Cellular and molecular life sciences : CMLS · 2015Review
- AKIP1, a cardiac hypertrophy induced protein that stimulates cardiomyocyte growth via the Akt pathway.International journal of molecular sciences · 2013Article
- Mitotic catastrophe triggered in human cancer cells by the viral protein apoptin.Cell death & disease · 2013Article
- PP2A-Mediated Anticancer Therapy.Gastroenterology research and practice · 2013Review
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptin (apoptosis-inducing protein) harbors tumor-selective characteristics making it a potential safe and effective anticancer agent. Apoptin becomes phosphorylated and induces apoptosis in a large panel of human tumor but not normal cells. Here, we used an in vitro oncogenic transformation assay to explore minimal cellular factors required for the activation of apoptin. Flag-apoptin was introduced into normal fibroblasts together with the transforming SV40 large T antigen (SV40 LT) and SV40 small t antigen (SV40 ST) antigens. We found that nuclear expression of SV40 ST in normal cells was sufficient to induce phosphorylation of apoptin. Mutational analysis showed that mutations disrupting the binding of ST to protein phosphatase 2A (PP2A) counteracted this effect. Knockdown of the ST-interacting PP2A-B56γ subunit in normal fibroblasts mimicked the effect of nuclear ST expression, resulting in induction of apoptin phosphorylation. The same effect was observed upon downregulation of the PP2A-B56δ subunit, which is targeted by protein kinase A (PKA). Apoptin interacts with the PKA-associating protein BCA3/AKIP1, and inhibition of PKA in tumor cells by treatment with H89 increased the phosphorylation of apoptin, whereas the PKA activator cAMP partially reduced it. We infer that inactivation of PP2A, in particular, of the B56γ and B56δ subunits is a crucial step in triggering apoptin-induced tumor-selective cell death.
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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 Socratic graph.