Model for regulation of MSMP expression in cancer cells and its proangiogenic role in ovarian tumors (Homo sapiens)
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Description
Proposed model for regulation of MSMP expression in cancer cells under hypoxic conditions and the proangiogenic role of MSMP in ovarian tumors.
The recruitment of the transcriptional repressor CTCF to the MSMP enhancer region is regulated by changes in H3 acetylation of the MSMP enhancer. In hypoxic conditions, the repressor-enhancer binding is disrupted, leading to increased expression of MSMP. Secretion of MSMP triggers MAPK signaling in endothelial cells (presumably via CCR2 signaling), which promotes angiogenesis.
This suggests that MSMP inhibition in combination with antiangiogenesis drugs (anti-VEGF) could be a new strategy to overcome resistance to antiangiogenesis therapy.
Description adapted from Mitamura et al.Quality Tags
Ontology Terms
Saving...Bibliography
- Mitamura T, Pradeep S, McGuire M, Wu SY, Ma S, Hatakeyama H, Lyons YA, Hisamatsu T, Noh K, Villar-Prados A, Chen X, Ivan C, Rodriguez-Aguayo C, Hu W, Lopez-Berestein G, Coleman RL, Sood AK; ''Induction of anti-VEGF therapy resistance by upregulated expression of microseminoprotein (MSMP).''; Oncogene, 2018 PubMed Europe PMC Scholia
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External references
DataNodes
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| Name | Type | Database reference | Comment |
|---|---|---|---|
| Angiogenesis | Pathway | WP1539 (WikiPathways)  | |
| CCR2 | GeneProduct | ENSG00000121807 (Ensembl) | |
| CTCF | GeneProduct | ENSG00000102974 (Ensembl) | |
| Hypoxia | Q105688 (Wikidata) | ||
| MAPK signaling | Pathway | WP382 (WikiPathways) | |
| MSMP | GeneProduct | ENSG00000215183 (Ensembl) |
Annotated Interactions
No annotated interactions
