ArticleCell cycle (Georgetown, Tex.)2020
Gain of function mutant p53 protein activates AKT through the Rac1 signaling to promote tumorigenesis.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Mutant p53Molecular oncology · 2026Article
- Regulation of autophagy by the p53 family and the implications for cancer therapies.Discover oncology · 2026Review
- Review
- Article
- SHMT2 promotes papillary thyroid cancer metastasis through epigenetic activation of AKT signaling.Cell death & disease · 2024Article
- TP53 to mediate immune escape in tumor microenvironment: an overview of the research progress.Molecular biology reports · 2024Review
- Development and validation of a vesicle-mediated transport-associated gene signature for predicting prognosis and immune therapy response in hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2023Article
- The Competition of Yin and Yang: Exploring the Role of Wild-Type and Mutant p53 in Tumor Progression.Biomedicines · 2023Article
- RHO GTPase family in hepatocellular carcinoma.Experimental hematology & oncology · 2022Review
- Article
- Rac1 as a Target to Treat Dysfunctions and Cancer of the Bladder.Biomedicines · 2022Review
- Article
- Mutant p53 achieved Gain-of-Function by promoting tumor growth and immune escape through PHLPP2/AKT/PD-L1 pathway.International journal of biological sciences · 2022Article
- Article
- Review
- Rac1/PAK1 signaling contributes to bone cancer pain by Regulation dendritic spine remodeling in rats.Molecular painArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor suppressor p53 is the most frequently mutated gene in human cancer. Mutant p53 (mutp53) not only loses the tumor suppressive activity of wild type p53, but often gains new oncogenic activities to promote tumorigenesis, defined as mutp53 gain of function (GOF). While the concept of mutp53 GOF is well-established, its underlying mechanism is not well-understood. AKT has been suggested to be activated by mutp53 and contribute to mutp53 GOF, but its underlying mechanism is unclear. In this study, we found that the activation of the Rac1 signaling by mutp53 mediates the promoting effect of mutp53 on AKT activation. Blocking Rac1 signaling by RNAi or a Rac1 inhibitor can inhibit AKT activation by mutp53. Importantly, targeting Rac1/AKT can greatly compromise mutp53 GOF in tumorigenesis. Results from this study uncover a new mechanism for AKT activation in tumors, and reveal that activation of AKT by mutp53
Indexed as
Identifiers
What 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.