ArticleSpringerPlus2015
The Ser/Thr kinase MAP4K4 drives c-Met-induced motility and invasiveness in a cell-based model of SHH medulloblastoma.
Article in SpringerPlus, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- A randomized, placebo-controlled, phase 1/2 study of tivantinib (ARQ 197) in combination with irinotecan and cetuximab in patients with metastatic colorectal cancer with wild-type KRAS who have received first-line systemic therapy.International journal of cancer · 2016Trial
- MAP4K4 regulates forces at cell-cell and cell-matrix adhesions to promote collective cell migration.Life science alliance · 2023Article
- Abrogation of MAP4K4 protein function causes congenital anomalies in humans and zebrafish.Science advances · 2023Article
- MAP4K4 and cancer: ready for the main stage?Frontiers in oncology · 2023Review
- ERRα coordinates actin and focal adhesion dynamics.Cancer gene therapy · 2022Article
- Cooperation of Striatin 3 and MAP4K4 promotes growth and tissue invasion.Communications biology · 2022Article
- Spatial proteomics finds CD155 and Endophilin-A1 as mediators of growth and invasion in medulloblastoma.Life science alliance · 2022Article
- The molecular basis of the dichotomous functionality of MAP4K4 in proliferation and cell motility control in cancer.Frontiers in oncology · 2022Review
- The hepatocyte growth factor/mesenchymal epithelial transition factor axis in high-risk pediatric solid tumors and the anti-tumor activity of targeted therapeutic agents.Frontiers in pediatrics · 2022Review
- HGK promotes metastatic dissemination in prostate cancer.Scientific reports · 2021Article
- CR13626: a novel oral brain penetrant tyrosine kinase inhibitor that reduces tumor growth and prolongs survival in a mouse model of glioblastoma.American journal of cancer research · 2021Article
- Mesenchymal Epithelial Transition Factor Signaling in Pediatric Nervous System Tumors: Implications for Malignancy and Cancer Stem Cell Enrichment.Frontiers in cell and developmental biology · 2021Review
- Real-time sensing of MAPK signaling in medulloblastoma cells reveals cellular evasion mechanism counteracting dasatinib blockade of ERK activation during invasion.Neoplasia (New York, N.Y.) · 2020Article
- MAP4K4 controlled integrin β1 activation and c-Met endocytosis are associated with invasive behavior of medulloblastoma cells.Oncotarget · 2018Article
- Role of exosomes in hepatocellular carcinoma cell mobility alteration.Oncology letters · 2017Article
- Investigation of brain tissue infiltration by medulloblastoma cells in an ex vivo model.Scientific reports · 2017Article
- Review
- Epigenetically regulated Fibronectin leucine rich transmembrane protein 2 (FLRT2) shows tumor suppressor activity in breast cancer cells.Scientific reports · 2017Article
- Computer-assisted quantification of motile and invasive capabilities of cancer cells.Scientific reports · 2015Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medulloblastoma (MB) comprises four molecularly and genetically distinct subgroups of embryonal brain tumors that develop in the cerebellum. MB mostly affects infants and children and is difficult to treat because of frequent dissemination of tumor cells within the leptomeningeal space. A potential promoter of cell dissemination is the c-Met proto-oncogene receptor tyrosine kinase, which is aberrantly expressed in many human tumors including MB. Database analysis showed that c-Met is highly expressed in the sonic hedgehog (SHH) subgroup and in a small subset of Group 3 and Group 4 MB tumors. Using a cell-based three-dimensional cell motility assay combined with live-cell imaging, we investigated whether the c-Met ligand HGF could drive dissemination of MB cells expressing high levels of c-Met, and determined downstream effector mechanisms of this process. We detected variable c-Met expression in different established human MB cell lines, and we found that in lines expressing high c-Met levels, HGF promoted cell dissemination and invasiveness. Specifically, HGF-induced c-Met activation enhanced the capability of the individual cells to migrate in a JNK-dependent manner. Additionally, we identified the Ser/Thr kinase MAP4K4 as a novel driver of c-Met-induced invasive cell dissemination. This increased invasive motility was due to MAP4K4 control of F-actin dynamics in structures required for migration and invasion. Thus, MAP4K4 couples growth factor signaling to actin cytoskeleton regulation in tumor cells, suggesting that MAP4K4 could present a promising novel target to be evaluated for treating growth factor-induced dissemination of MB tumors of different subgroups and of other human cancers.
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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.