ArticleOncology letters2016
Power of PTEN/AKT: Molecular switch between tumor suppressors and oncogenes.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 52 citations in OpenAlex.
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- Research progress of drug resistance mechanism of temozolomide in the treatment of glioblastoma.Heliyon · 2024Review
- TNFα-Induced Altered miRNA Expression Links to NF-κB Signaling Pathway in Endometriosis.Inflammation · 2023Article
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- TNFα-induced altered miRNA expression links to NF-κB signaling pathway in endometriosis.Research square · 2023Article
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- Inhibition of lncRNA RET enhances radio-sensitivity of tumor cells via miR-3179/Slug/PTEN axis.Toxicology research · 2022Article
- Article
- Insulin Resistance and Cancer: In Search for a Causal Link.International journal of molecular sciences · 2021Review
- MicroRNAs: The Link between the Metabolic Syndrome and Oncogenesis.International journal of molecular sciences · 2021Review
- Mass Spectrometry Imaging of Fibroblasts: Promise and Challenge.Expert review of proteomics · 2021Review
- Expression and clinical significance of microRNA-21, PTEN and p27 in cancer tissues of patients with non-small cell lung cancer.Oncology letters · 2020Article
- Ras Suppressor-1 (RSU1) in Cancer Cell Metastasis: A Tale of a Tumor Suppressor.International journal of molecular sciences · 2020Review
- Per2 attenuates LPS-induced chondrocyte injury through the PTEN/PI3K/Akt signalling pathway.Bioscience reports · 2020Article
- Rapamycin enhanced the antitumor effects of doxorubicin in myelogenous leukemia K562 cells by downregulating the mTOR/p70S6K pathway.Oncology letters · 2019Article
- Effect of microRNA-29b on proliferation, migration, and invasion of endometrial cancer cells.The Journal of international medical research · 2019Article
- AKT/protein kinase B associates with β-actin in the nucleus of melanoma cells.Bioscience reports · 2019Article
- Systematic analysis of NLMP suggests nuclear localization of RTK/MET kinases resemble cancer cell clearance.Journal of experimental & clinical cancer research : CR · 2019Article
- MicroRNA-423 promotes proliferation, migration and invasion and induces chemoresistance of endometrial cancer cells.Experimental and therapeutic medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increasing amount of evidence has shown that tumor suppressors can become oncogenes, or vice versa, but the mechanism behind this is unclear. Recent findings have suggested that phosphatase and tensin homolog (PTEN) is one of the powerful switches for the conversion between tumor suppressors and oncogenes. PTEN regulates a number of cellular processes, including cell death and proliferation, through the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. Furthermore, a number of studies have suggested that PTEN deletions may alter various functions of certain tumor suppressor and oncogenic proteins. The aim of the present review was to analyze specific cases driven by PTEN loss/AKT activation, including aberrant signaling pathways and novel drug targets for clinical application in personalized medicine. The findings illustrate how PTEN loss and/or AKT activation switches MDM2-dependent p53 downregulation, and induces conversion between oncogene and tumor suppressor in enhancer of zeste homolog 2, BTB domain-containing 7A, alternative reading frame 2, p27 and breast cancer 1, early onset, through multiple mechanisms. This review highlights the genetic basis of complex drug targets and provides insights into the rationale of precision cancer therapy.
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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 OpenQuestion graph.