Disease relevance of SEMA3C

• Further, all glioma cell lines express SEMA3A and SEMA3C and exhibit SEMA3A binding sites [1].
• Correlation of MDR-1, nm23-H1 and H Sema E gene expression with histopathological findings and clinical outcome in ovarian and breast cancer patients [2].
• Group 2 genes are normally down-regulated during the window of implantation but are significantly increased with endometriosis: semaphorin E, neuronal olfactomedin-related endoplasmic reticulum localized protein mRNA and Sam68-like phosphotyrosine protein alpha [3].

High impact information on SEMA3C

• After repeated CDDP selection, cDNA homologous to murine semaphorin E was isolated from surviving cells [4].
• Human semaphorin E (H-sema E) was overexpressed in CDDP-resistant cell lines and was readily induced not only by diverse chemotherapeutic drugs but also by x-ray and UV irradiation [4].
• Identification of semaphorin E as a non-MDR drug resistance gene of human cancers [4].
• The novel genes, including caveolin-1, semaphorin E, and FMS-like tyrosine kinase 3 ligand, have putative roles in carcinogenesis but have not been reported in hepatocellular carcinogenesis [5].
• Identification of human semaphorin E gene expression in rheumatoid synovial cells by mRNA differential display [6].

Biological context of SEMA3C

• We identified an upregulation of the human semaphorin E gene in rheumatoid synovial fibroblastoid cells [6].

Other interactions of SEMA3C

• The majority of specimens were found to be positive for MDR-1 and H Sema E gene expression, while nm23-H1 was detected in less than 50% of the patients [2].

References