ArticleOncotarget2014
Loss of PTEN stabilizes the lipid modifying enzyme cytosolic phospholipase A₂α via AKT in prostate cancer cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Cavin gene family and caveolae-related disorders: pathogenetic roles and possible mechanisms.Cell communication and signaling : CCS · 2026Review
- VLCAD inhibits the proliferation and invasion of hepatocellular cancer cells through regulating PI3K/AKT axis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- The diversity and breadth of cancer cell fatty acid metabolism.Cancer & metabolism · 2021Review
- Myeloid-derived cells in prostate cancer progression: phenotype and prospective therapies.Journal of leukocyte biology · 2017Review
- Withaferin A Inhibits Prostate Carcinogenesis in a PTEN-deficient Mouse Model of Prostate Cancer.Neoplasia (New York, N.Y.) · 2017Article
- cPLA2α mediates TGF-β-induced epithelial-mesenchymal transition in breast cancer through PI3k/Akt signaling.Cell death & disease · 2017Article
- Global or Granulosa Cell-Specific Pten Mutations in Combination with Elevated FSH Levels Fail to Cause Ovarian Tumours in Mice.Hormones & cancer · 2016Article
- Probing the PI3K/Akt/mTor pathway usingScientific reports · 2016Article
- Guttiferone K impedes cell cycle re-entry of quiescent prostate cancer cells via stabilization of FBXW7 and subsequent c-MYC degradation.Cell death & disease · 2016Article
- A simple, accurate and universal method for quantification of PCR.BMC biotechnology · 2016Article
- Discrete functions of GSK3α and GSK3β isoforms in prostate tumor growth and micrometastasis.Oncotarget · 2015Article
- Cathelicidin, an antimicrobial peptide produced by macrophages, promotes colon cancer by activating the Wnt/β-catenin pathway.Oncotarget · 2015Article
- ClC-3 chloride channel modulates the proliferation and migration of osteosarcoma cells via AKT/GSK3β signaling pathway.International journal of clinical and experimental pathology · 2015Article
- Targeting cytosolic phospholipase A2 α in colorectal cancer cells inhibits constitutively activated protein kinase B (AKT) and cell proliferation.Oncotarget · 2014Article
- Signaling pathways activation profiles make better markers of cancer than expression of individual genes.Oncotarget · 2014Article
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 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant increase in pAKT, due to a gain-of-function mutation of PI3K or loss-of-function mutation or deletion of PTEN, occurs in prostate cancer and is associated with poor patient prognosis. Cytosolic phospholipase A₂α (cPLA₂α) is a lipid modifying enzyme by catalyzing the hydrolysis of membrane arachidonic acid. Arachidonic acid and its metabolites contribute to survival and proliferation of prostate cancer cells. We examined whether AKT plays a role in promoting cPLA₂α action in prostate cancer cells. We found a concordant increase in pAKT and cPLA₂α levels in prostate tissue of prostate epithelial-specific PTEN-knockout but not PTEN-wide type mice. Restoration of PTEN expression or inhibition of PI3K action decreased cPLA₂α expression in PTEN-mutated or deleted prostate cancer cells. An increase in AKT by Myr-AKT elevated cPLA₂α protein levels, which could be diminished by inhibition of AKT phosphorylation without noticeable change in total AKT levels. pAKT levels had no influence on cPLA₂α at mRNA levels but reduced cPLA₂α protein degradation. Anti-AKT antibody co-immunoprecipitated cPLA₂α and vice versa. Hence, AKT plays a role in enhancing cPLA₂α protein stability in PTEN-null prostate cancer cells, revealing a link between oncogenic pathway and lipid metabolism.
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.