ARHGEF10L Promotes Cervical Tumorigenesis via RhoA-Mediated Signaling.
Junyi TangKehua FangChang LiXiaotian ChangPublished in: Evidence-based complementary and alternative medicine : eCAM (2021)
ARHGEF10L overexpression promoted cell proliferation and migration, reduced cell apoptosis, and induced epithelial-to-mesenchymal transition (EMT) via downregulation of E-cadherin and upregulation of N-cadherin and Slug in transfected HeLa cells. The overexpression of ARHGEF10L also upregulated GTP-RhoA, ROCK1, and phospho-ezrin/radixin/moesin (ERM) expression in HeLa cells. RNA-sequencing analysis detected altered transcription of 31 genes in HeLa cells with ARHGEF10L overexpression. Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene ontology (GO) pathway analyses identified significant differences in cyclin-dependent protein serine/threonine kinase activity, cell responses to vitamin A, and Toll-like receptor signaling pathways. Both real-time PCR and Western blotting verified the increased expression of heat shock 70 kDa protein 6 (HSPA6) in ARHGEF10L-overexpressing HeLa cells. Since we reported that ARHGEF10L played a role through RhoA-ROCK1-ERM signaling, an important pathway in tumorigenesis, and stimulated EMT and HSPA6 expression in liver tumors and gastric tumor cells, we suggest that ARHGEF10L is a novel oncogene in many tumors.
Keyphrases
- cell cycle arrest
- induced apoptosis
- cell proliferation
- cell death
- poor prognosis
- signaling pathway
- toll like receptor
- pi k akt
- epithelial mesenchymal transition
- single cell
- heat shock
- endoplasmic reticulum stress
- transcription factor
- heat shock protein
- genome wide
- binding protein
- inflammatory response
- protein kinase
- cell cycle
- small molecule
- dna methylation
- gene expression
- south africa
- cell adhesion