{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ungefroren H"],"funding":["Canadian Institutes of Health Research"],"pagination":["E691"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6562819"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(5)"],"pubmed_abstract":["The small GTPase Ras-related C3 botulinum toxin substrate 1B (RAC1B) has been shown previously by RNA interference-mediated knockdown (KD) to function as a powerful inhibitor of transforming growth factor (TGF)-β1-induced cell migration and epithelial-mesenchymal transition in epithelial cells, but the underlying mechanism has remained enigmatic. Using pancreatic carcinoma cells, we show that both KD and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9-mediated knockout (KO) of RAC1B increased the expression of the TGF-β type I receptor ALK5 (activin receptor-like kinase 5), but this effect was more pronounced in CRISPR-KO cells. Of note, in KO, but not KD cells, ALK5 upregulation was associated with resensitization of TGFBR1 to induction by TGF-β1 stimulation. RAC1B"],"journal":["Cancers"],"pubmed_title":["RAC1B Suppresses TGF-β1-Dependent Cell Migration in Pancreatic Carcinoma Cells through Inhibition of the TGF-β Type I Receptor ALK5."],"pmcid":["PMC6562819"],"funding_grant_id":["PJT148565 to M.D.H."],"pubmed_authors":["Mihara K","Gieseler F","Witte D","Hollenberg MD","Fiedler C","Otterbein H","Lehnert H","Ungefroren H"],"additional_accession":[]},"is_claimable":false,"name":"RAC1B Suppresses TGF-β1-Dependent Cell Migration in Pancreatic Carcinoma Cells through Inhibition of the TGF-β Type I Receptor ALK5.","description":"The small GTPase Ras-related C3 botulinum toxin substrate 1B (RAC1B) has been shown previously by RNA interference-mediated knockdown (KD) to function as a powerful inhibitor of transforming growth factor (TGF)-β1-induced cell migration and epithelial-mesenchymal transition in epithelial cells, but the underlying mechanism has remained enigmatic. Using pancreatic carcinoma cells, we show that both KD and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9-mediated knockout (KO) of RAC1B increased the expression of the TGF-β type I receptor ALK5 (activin receptor-like kinase 5), but this effect was more pronounced in CRISPR-KO cells. Of note, in KO, but not KD cells, ALK5 upregulation was associated with resensitization of TGFBR1 to induction by TGF-β1 stimulation. RAC1B","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 May","modification":"2025-04-05T10:41:26.436Z","creation":"2019-07-24T07:16:25Z"},"accession":"S-EPMC6562819","cross_references":{"pubmed":["31108998"],"doi":["10.3390/cancers11050691"]}}