ArticleMolecular cancer2017
Role of MEK partner-1 in cancer stemness through MEK/ERK pathway in cancerous neural stem cells, expressing EGFRviii.
Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Atypical cyclin P regulates cancer cell stemness through activation of the WNT pathway.Cellular oncology (Dordrecht, Netherlands) · 2021Article
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- Circ_0075829 facilitates the progression of pancreatic carcinoma by sponging miR-1287-5p and activating LAMTOR3 signalling.Journal of cellular and molecular medicine · 2020Article
- ERK-mediated negative feedback regulation of oncogenic EGFRvIII in glioblastoma cells.Oncology letters · 2020Article
- Article
- Gaps and Doubts in Search to Recognize Glioblastoma Cellular Origin and Tumor Initiating Cells.Journal of oncology · 2020Review
- Pre-clinical evidences for the efficacy of tryptanthrin as a potent suppressor of skin cancer.Cell proliferation · 2020Article
- Enhanced Hsa-miR-181d/p-STAT3 and Hsa-miR-181d/p-STAT5A Ratios Mediate the Anticancer Effect of Garcinol inCancers · 2019Article
- Transcriptional factor six2 promotes the competitive endogenous RNA network between CYP4Z1 and pseudogene CYP4Z2P responsible for maintaining the stemness of breast cancer cells.Journal of hematology & oncology · 2019Article
- Cancer Stem Cells in Neuroblastoma: Expanding the Therapeutic Frontier.Frontiers in molecular neuroscience · 2019Review
- Antagonistic role of GSK3 isoforms in glioma survival.Journal of Cancer · 2018Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioma stem cells (GSCs) are a major cause of the frequent relapse observed in glioma, due to their high drug resistance and their differentiation potential. Therefore, understanding the molecular mechanisms governing the 'cancer stemness' of GSCs will be particularly important for improving the prognosis of glioma patients.
methodsWe previously established cancerous neural stem cells (CNSCs) from immortalized human neural stem cells (F3 cells), using the H-Ras oncogene. In this study, we utilized the EGFRviii mutation, which frequently occurs in brain cancers, to establish another CNSC line (F3.EGFRviii), and characterized its stemness under spheroid culture.
resultsThe F3.EGFRviii cell line was highly tumorigenic in vitro and showed high ERK1/2 activity as well as expression of a variety of genes associated with cancer stemness, such as SOX2 and NANOG, under spheroid culture conditions. Through meta-analysis, PCR super-array, and subsequent biochemical assays, the induction of MEK partner-1 (MP1, encoded by the LAMTOR3 gene) was shown to play an important role in maintaining ERK1/2 activity during the acquisition of cancer stemness under spheroid culture conditions. High expression of this gene was also closely associated with poor prognosis in brain cancer.
conclusionThese data suggest that MP1 contributes to cancer stemness in EGFRviii-expressing glioma cells by driving ERK activity.
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