ArticleHepatology (Baltimore, Md.)2013
MAT2B-GIT1 interplay activates MEK1/ERK 1 and 2 to induce growth in human liver and colon cancer.
Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 81 citations in OpenAlex.
- A small molecule inhibitor of ARF GTPase protein 1 limits liver and colon cancer cell growth and metastasis.Cell death & disease · 2026Article
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- Molecular characterization of positively selected genes contributing aquatic adaptation in marine mammals.Genes & genomics · 2024Article
- Physical activity and exercise in liver cancer.Liver research (Beijing, China) · 2024Review
- MEK1-dependent MondoA phosphorylation regulates glucose uptake in response to ketone bodies in colorectal cancer cells.Cancer science · 2023Article
- Article
- Construction of a synthetic methodology-based library and its application in identifying a GIT/PIX protein-protein interaction inhibitor.Nature communications · 2022Article
- GIT1 protects against breast cancer growth through negative regulation of Notch.Nature communications · 2022Article
- Review
- Mutual Correlation between Non-Coding RNA and S-Adenosylmethionine in Human Cancer: Roles and Therapeutic Opportunities.Cancers · 2021Review
- Article
- Decreased long non-coding RNA lincFOXF1 indicates poor progression and promotes cell migration and metastasis in osteosarcoma.Journal of cellular and molecular medicine · 2020Article
- Macrophage GIT1 Contributes to Bone Regeneration by Regulating Inflammatory Responses in an ERK/NRF2-Dependent Way.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- The Arf-GAP and protein scaffold Cat1/Git1 as a multifaceted regulator of cancer progression.Small GTPases · 2020Review
- AGAP2: Modulating TGFβ1-Signaling in the Regulation of Liver Fibrosis.International journal of molecular sciences · 2020Review
- The Role of ARF Family Proteins and Their Regulators and Effectors in Cancer Progression: A Therapeutic Perspective.Frontiers in cell and developmental biology · 2020Review
- MAT2B mediates invasion and metastasis by regulating EGFR signaling pathway in hepatocellular carcinoma.Clinical and experimental medicine · 2019Article
- Methionine adenosyltransferases in liver cancer.World journal of gastroenterology · 2019Review
- MAT2B promotes proliferation and inhibits apoptosis in osteosarcoma by targeting epidermal growth factor receptor and proliferating cell nuclear antigen.International journal of oncology · 2019Article
- Antisense Oligonucleotides against miR-21 Inhibit the Growth and Metastasis of Colorectal Carcinoma via the DUSP8 Pathway.Molecular therapy. Nucleic acids · 2018Article
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
unlabelledMethionine adenosyltransferase 2B (MAT2B) encodes for two variant proteins (V1 and V2) that promote cell growth. Using in-solution proteomics, GIT1 (G Protein Coupled Receptor Kinase Interacting ArfGAP 1) was identified as a potential interacting partner of MAT2B. Here, we examined the functional significance of this interplay. Coimmunoprecipitation experiments examined protein interactions. Tissue expression levels of proteins were examined using immunohistochemistry and western blotting. Expression levels of proteins were varied using transient knockdown or overexpression to observe the effect of alterations in each protein on the entire complex. Direct interaction among individual proteins was further verified using in vitro translated and recombinant proteins. We found both MAT2B variants interact with GIT1. Overexpression of V1, V2, or GIT1 activated mitogen-activated protein kinase kinase 1 (MEK1) and extracellular signal-regulated kinase (ERK), raised cyclin D1 protein level, and increased growth, whereas the opposite occurred when V1, V2, or GIT1 was knocked down. MAT2B and GIT1 require each other to activate MEK1/ERK and increase growth. MAT2B directly interacts with MEK1, GIT1, and ERK2. Expression level of V1, V2, or GIT1 directly influenced recruitment of GIT1 or MAT2B and ERK2 to MEK1, respectively. In pull-down assays, MAT2B directly promoted binding of GIT1 and ERK2 to MEK1. MAT2B and GIT1 interact and are overexpressed in most human liver and colon cancer specimens. Increased expression of V1, V2, or GIT1 promoted growth in an orthotopic liver cancer model, whereas increased expression of either V1 or V2 with GIT1 further enhanced growth and lung metastasis.
conclusionMAT2B and GIT1 form a scaffold, which recruits and activates MEK and ERK to promote growth and tumorigenesis. This novel MAT2B/GIT1 complex may provide a potential therapeutic gateway in human liver and colon cancer. (HEPATOLOGY 2012).
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