CDB25:0004260 SEMA3C — PLXNB1

Experimentally validated in Human; Orthology-inferred in Mouse, Rat, Frog, Zebrafish, Chicken, Macaque, Pig, Dog, Cow, Chimp, Horse, Marmoset, Sheep

Title

Journal:; Year Published:

Abstract

SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1.

EMBO molecular medicine, 2018; PubMed, Homo sapiens SEMA3C — Homo sapiens PLXNB1
ABSTRACT: Growth factor receptor tyrosine kinase (RTK) pathway activation is a key mechanism for mediating cancer growth, survival, and treatment resistance. Cognate ligands play crucial roles in autocrine or paracrine stimulation of these RTK pathways. Here, we show SEMA3C drives activation of multiple RTKs including EGFR, ErbB2, and MET in a cognate ligand-independent manner via Plexin B1. SEMA3C expression levels increase in castration-resistant prostate cancer (CRPC), where it functions to promote cancer cell growth and resistance to androgen receptor pathway inhibition. SEMA3C inhibition delays CRPC and enzalutamide-resistant progression. Plexin B1 sema domain-containing:Fc fusion proteins suppress RTK signaling and cell growth and inhibit CRPC progression of LNCaP xenografts post-castration in vivo SEMA3C inhibition represents a novel therapeutic strategy for treatment of advanced prostate cancer.
Basic Information on SEMA3C
Ligand Name: semaphorin 3C
Other Symbols: SEMAE, SemE
Ligand Location: secreted based on hpa, perplexity, uniprot, cell membrane based on hpa
HGNC Gene Symbol Report: SEMA3C
GeneCards: SEMA3C
Interactions with other Receptors for SEMA3C
Basic Information on PLXNB1
Receptor Name: plexin B1
Other Symbols: PLXN5, SEP, KIAA0407
Receptor Location: cell membrane based on perplexity, uniprot
HGNC Gene Symbol Report: PLXNB1
GeneCards: PLXNB1
HGNC Gene Group: IPT domain containing, Plexins
Interactions with other Ligands for PLXNB1