ArticleeLife2015
Greatwall promotes cell transformation by hyperactivating AKT in human malignancies.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 58 citations in OpenAlex.
- Greatwall kinase regulates acute myeloid leukaemia cell division through a non-canonical mechanism.EMBO reports · 2026Article
- Therapeutic potential of targeting MASTL in lung adenocarcinoma.Scientific reports · 2026Article
- MASTL Promotes Hepatocellular Carcinoma Progression and Paclitaxel Resistance Through Mitotic Catastrophe.Cancer science · 2026Article
- The balance between B55α and Greatwall expression levels predicts sensitivity to Greatwall inhibition in cancer cells.Nature communications · 2025Article
- Activity-based protein profiling and global proteome analysis reveal MASTL as a potential therapeutic target in gastric cancer.Cell communication and signaling : CCS · 2024Article
- IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Novel Roles of the Greatwall Kinase Rim15 in Yeast Oxidative Stress Tolerance through Mediating Antioxidant Systems and Transcriptional Regulation.Antioxidants (Basel, Switzerland) · 2024Article
- The value of chromosome instability detected by low-pass whole-genome sequencing in preoperative prediction of sentinel lymph node metastasis in breast cancer.Frontiers in oncology · 2024Article
- Histone H3 serine-57 is a CHK1 substrate whose phosphorylation affects DNA repair.Nature communications · 2023Article
- The MASTL/PP2A cell cycle kinase-phosphatase module restrains PI3K-Akt activity in an mTORC1-dependent manner.The EMBO journal · 2023Article
- SILAC kinase screen identifies potential MASTL substrates.Scientific reports · 2022Article
- MASTL is enriched in cancerous and pluripotent stem cells and influences OCT1/OCT4 levels.iScience · 2022Article
- Therapeutic natural compounds Enzastaurin and Palbociclib inhibit MASTL kinase activity preventing breast cancer cell proliferation.Medical oncology (Northwood, London, England) · 2022Article
- The MASTL-ENSA-PP2A/B55 axis modulates cisplatin resistance in oral squamous cell carcinoma.Frontiers in cell and developmental biology · 2022Article
- Identification of Key microRNAs and Genes in Infantile Hemangiomas.Frontiers in genetics · 2022Article
- Article
- Discovery and Characterization of a Novel MASTL Inhibitor MKI-2 Targeting MASTL-PP2A in Breast Cancer Cells and Oocytes.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Mechanical Control of Cell Migration by the Metastasis Suppressor Tetraspanin CD82/KAI1.Cells · 2021Article
- Knockdown of Microtubule Associated Serine/threonine Kinase Like Expression Inhibits Gastric Cancer Cell Growth and Induces Apoptosis by Activation of ERK1/2 and Inactivation of NF-κB Signaling.Current medical science · 2021Article
- PP2A-B55 Holoenzyme Regulation and Cancer.Biomolecules · 2020Review
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PP2A phosphatase is often inactivated in cancer and is considered as a tumour suppressor. A new pathway controlling PP2A activity in mitosis has been recently described. This pathway includes the Greatwall (GWL) kinase and its substrates endosulfines. At mitotic entry, GWL is activated and phosphorylates endosulfines that then bind and inhibit PP2A. We analysed whether GWL overexpression could participate in cancer development. We show that GWL overexpression promotes cell transformation and increases invasive capacities of cells through hyperphosphorylation of the oncogenic kinase AKT. Interestingly, AKT hyperphosphorylation induced by GWL is independent of endosulfines. Rather, GWL induces GSK3 kinase dephosphorylation in its inhibitory sites and subsequent SCF-dependent degradation of the PHLPP phosphatase responsible for AKT dephosphorylation. In line with its oncogenic activity, we find that GWL is often overexpressed in human colorectal tumoral tissues. Thus, GWL is a human oncoprotein that promotes the hyperactivation of AKT via the degradation of its phosphatase, PHLPP, in human malignancies.
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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.