ArticleCell communication and signaling : CCS2018
Reduced menin expression impairs rapamycin effects as evidenced by an increase in mTORC2 signaling and cell migration.
Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Menin in Cancer.Genes · 2024Review
- The link between menin and pleiotrophin in the tumor biology of pancreatic neuroendocrine neoplasms.Cancer science · 2022Article
- Multiple endocrine neoplasia type 1 combined with thyroid neoplasm: A case report and review of literatures.World journal of clinical cases · 2022Article
- CDK7 blockade suppresses super-enhancer-associated oncogenes in bladder cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Generation and characterization of CRISPR/Cas9-mediated MEN1 knockout BON1 cells: a human pancreatic neuroendocrine cell line.Scientific reports · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMammalian target of rapamycin (mTOR) is a master regulator of various cellular responses by forming two functional complexes, mTORC1 and mTORC2. mTOR signaling is frequently dysregulated in pancreatic neuroendocrine tumors (PNETs). mTOR inhibitors have been used in attempts to treat these lesions, and prolonged progression free survival has been recorded. If this holds true also for the multiple endocrine neoplasia type 1 (MEN1) associated PNETs is yet unclear. We investigated the relationship between expression of the MEN1 protein menin and mTOR signaling in the presence or absence of the mTOR inhibitor rapamycin.
methodsIn addition to use of menin wild type and menin-null mouse embryonic fibroblasts (MEFs), menin was silenced by siRNA in pancreatic neuroendocrine tumor cell line BON-1. Panels of protein phosphorylation, as activation markers downstream of PI3k-mTOR-Akt pathways, as well as menin expression were evaluated by immunoblotting. The impact of menin expression in the presence and absence of rapamycin was determinate upon Wound healing, migration and proliferation in MEFs and BON1 cells.
resultsPDGF-BB markedly increased phosphorylation of mTORC2 substrate Akt, at serine 473 (S473) and threonine 450 (T450) in menin
conclusionsMenin is involved in regulatory mechanism between the two mTOR complexes, and its reduced expression is accompanied with increased mTORC2-Akt signaling, which consequently impairs anti-migratory effect of rapamycin.
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