ArticlePloS one2013
Attenuated expression of apoptosis stimulating protein of p53-2 (ASPP2) in human acute leukemia is associated with therapy failure.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- High iASPP (PPP1R13L) expression is an independent predictor of adverse clinical outcome in acute myeloid leukemia (AML).Cell death & disease · 2024Article
- Evaluation of apoptosis stimulating protein of TP53-1 (ASPP1/PPP1R13B) to predict therapy resistance and overall survival in acute myeloid leukemia (AML).Cell death & disease · 2024Article
- miR-21 Targets ASPP2 to Inhibit Apoptosis via CHOP-Mediated Signaling inJournal of oncology · 2023Article
- ASPP2 promotes cell apoptosis in cervical cancer through inhibiting autophagy.Experimental and therapeutic medicine · 2022Article
- Article
- ASPP2κ Is Expressed In Human Colorectal Carcinoma And Promotes Chemotherapy Resistance And Tumorigenesis.Frontiers in molecular biosciences · 2021Article
- Alternative splicing of the tumor suppressor ASPP2 results in a stress-inducible, oncogenic isoform prevalent in acute leukemia.EBioMedicine · 2019Article
- Expression and significance of ASPP2 in squamous carcinoma of esophagus.The Kaohsiung journal of medical sciences · 2018Article
- The family of apoptosis-stimulating proteins of p53 is dysregulated in colorectal cancer patients.Oncology letters · 2018Article
- DNA methylation in silkworm genome may provide insights into epigenetic regulation of response to Bombyx mori cypovirus infection.Scientific reports · 2017Article
- ΔN-ASPP2, a novel isoform of the ASPP2 tumor suppressor, promotes cellular survival.Biochemical and biophysical research communications · 2017Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivation of the p53 pathway is a universal event in human cancers and promotes tumorigenesis and resistance to chemotherapy. Inactivating p53 mutations are uncommon in non-complex karyotype leukemias, thus the p53-pathway must be inactivated by other mechanisms. The Apoptosis Stimulating Protein of p53-2 (ASPP2) is a damage-inducible p53-binding protein that enhances apoptosis at least in part through a p53-mediated pathway. We have previously shown, that ASPP2 is an independent haploinsufficient tumor suppressor in vivo. Now, we reveal that ASPP2 expression is significantly attenuated in acute myeloid and lymphoid leukemia - especially in patients with an unfavorable prognostic risk profile and patients who fail induction chemotherapy. In line, knock down of ASPP2 in expressing leukemia cell lines and native leukemic blasts attenuates damage-induced apoptosis. Furthermore, cultured blasts derived from high-risk leukemias fail to induce ASPP2 expression upon anthracycline treatment. The mechanisms of ASPP2 dysregulation are unknown. We provide evidence that attenuation of ASPP2 is caused by hypermethylation of the promoter and 5'UTR regions in native leukemia blasts. Together, our results suggest that ASPP2 contributes to the biology of leukemia and expression should be further explored as a potential prognostic and/or predictive biomarker to monitor therapy responses in acute leukemia.
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