ArticleAmerican journal of cancer research2018
DLC2 inhibits development of glioma through regulating the expression ratio of TAp73α/TAp73β.
Article in American journal of cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- Regulatory mechanisms and potential medical applications of HNF1A-AS1 in cancers.American journal of translational research · 2022Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- STARD3: A Prospective Target for Cancer Therapy.Cancers · 2021Review
- Integrative analysis of TP73 profile prognostic significance in WHO grade II/III glioma.Cancer medicine · 2021Article
- StarD13: a potential star target for tumor therapeutics.Human cell · 2020Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To date, the anti-tumor mechanism of the deleted in liver cancer 2 (DLC2) in gliomas is still unclear. The study shows that TAp73α expression and TAp73α/TAp73β ratio are frequently high in gliomas and that TAp73α and TAp73β have opposite roles in regulating proliferation and apoptosis of glioma cells. Moreover, DLC2 is low-expressed in gliomas, which negatively correlates with TAp73α expression and TAp73α/TAp73β ratio. More importantly, DLC2 inhibits development of glioma by decreasing expression of TAp73α, which changes the expression ratio of TAp73α/TAp73β in glioma cells. Mechanically, DLC2 interacts directly with TAp73α and induces TAp73α ubiquitination and degradation, which is mediated through SAM domain of DLC2 and TAp73α. In detail, DLC2 with SAM domain deletion fails to interact with TAp73α and induce TAp73α ubiquitination and degradation, and SAM deletion decreased tumorigenesis-inhibition effect of DLC2. In conclusion, DLC2 inhibits glioma development by inducing TAp73α degradation and subsequent change of TAp73α/TAp73β expression ratio.
Indexed as
Identifiers
30094094PMC6079157What OpenQuestion holds
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.