{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yu H"],"funding":["Japan Society for the Promotion of Science"],"pagination":["3013-3025"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11462976"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["115(9)"],"pubmed_abstract":["RECK has been described to modulate extracellular matrix components through negative regulation of MMP activities. Recently, RECK was demonstrated to bind to an orphan G protein-coupled receptor GPR124 to mediate WNT7 signaling in nontumor contexts. Here, we attempted to clarify the role of RECK in driving WNT signaling in cancer cells. RECK and GPR124 formed a complex in 293T cells, and when both were expressed, WNT signaling was significantly enhanced in a WNT7-dependent manner. This cooperation was abolished when RECK mutants unable to bind to GPR124 were transduced. RECK stimulated the growth of KRAS-mutated pancreatic ductal adenocarcinoma (PDAC) cells with increased sensitivity to WNT inhibitor in a GPR124-dependent manner. A gastric cancer cell line SH10TC endogenously expresses bot"],"journal":["Cancer science"],"pubmed_title":["RECK/GPR124-driven WNT signaling in pancreatic and gastric cancer cells."],"pmcid":["PMC11462976"],"funding_grant_id":["19K22555","20H03509"],"pubmed_authors":["Takegami Y","Kohno S","Nakayama J","Takahashi C","Zhang Y","Voon DC","Hussein NH","Yu H"],"additional_accession":[]},"is_claimable":false,"name":"RECK/GPR124-driven WNT signaling in pancreatic and gastric cancer cells.","description":"RECK has been described to modulate extracellular matrix components through negative regulation of MMP activities. Recently, RECK was demonstrated to bind to an orphan G protein-coupled receptor GPR124 to mediate WNT7 signaling in nontumor contexts. Here, we attempted to clarify the role of RECK in driving WNT signaling in cancer cells. RECK and GPR124 formed a complex in 293T cells, and when both were expressed, WNT signaling was significantly enhanced in a WNT7-dependent manner. This cooperation was abolished when RECK mutants unable to bind to GPR124 were transduced. RECK stimulated the growth of KRAS-mutated pancreatic ductal adenocarcinoma (PDAC) cells with increased sensitivity to WNT inhibitor in a GPR124-dependent manner. A gastric cancer cell line SH10TC endogenously expresses bot","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-07-14T19:40:35.55Z","creation":"2025-04-19T19:25:22.5Z"},"accession":"S-EPMC11462976","cross_references":{"pubmed":["38923741"],"doi":["10.1111/cas.16258"]}}