Model for regulation of MSMP expression in cancer cells and its proangiogenic role in ovarian tumors (WP4397)

Homo sapiens

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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.

Authors

Kristina Hanspers , Friederike Ehrhart , Egon Willighagen , and Eric Weitz

Activity

last edited

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Organisms

Homo sapiens

Communities

CPTAC ExRNA

Annotations

Pathway Ontology

CC chemokine mediated signaling pathway cancer pathway

Disease Ontology

ovarian cancer

Cell Type Ontology

neoplastic cell endothelial cell

Participants
Query Drugst.One

Label Type Compact URI Comment
CCR2 GeneProduct ensembl:ENSG00000121807
MSMP GeneProduct ensembl:ENSG00000215183
CTCF GeneProduct ensembl:ENSG00000102974

References

  1. Induction of anti-VEGF therapy resistance by upregulated expression of microseminoprotein (MSMP). Mitamura T, Pradeep S, McGuire M, Wu SY, Ma S, Hatakeyama H, et al. Oncogene. 2018 Feb 8;37(6):722–31. PubMed Europe PMC Scholia