{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mancarella S"],"funding":["Ministero della Salute","Fondazione AIRC per la ricerca sul cancro ETS"],"pagination":["286"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11484308"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["43(1)"],"pubmed_abstract":["<h4>Background</h4>Cancer-associated fibroblasts (CAFs), mainly responsible for the desmoplastic reaction hallmark of intrahepatic Cholangiocarcinoma (iCCA), likely have a role in tumor aggressiveness and resistance to therapy, although the molecular mechanisms involved are unknown. Aim of the study is to investigate how targeting hCAF/iCCA cross-talk with a Notch1 inhibitor, namely Crenigacestat, may affect cancer progression.<h4>Methods</h4>We used different in vitro models in 2D and established new 3D hetero-spheroids with iCCA cells and human (h)CAFs. The results were confirmed in a xenograft model, and explanted tumoral tissues underwent transcriptomic and bioinformatic analysis.<h4>Results</h4>hCAFs/iCCA cross-talk sustains increased migration of both KKU-M213 and KKU-M156 cells, whi"],"journal":["Journal of experimental & clinical cancer research : CR"],"pubmed_title":["Targeting cancer-associated fibroblasts/tumor cells cross-talk inhibits intrahepatic cholangiocarcinoma progression via cell-cycle arrest."],"pmcid":["PMC11484308"],"funding_grant_id":["Ricerca Corrente 2024","IG 2020 ID 24815"],"pubmed_authors":["Pizzuto E","De Bellis M","Ardito F","Terzi A","Dituri F","Vincenti L","Maiorano E","Mancarella S","Serino G","Calvisi DF","Giannelli G","Gigante I"],"additional_accession":[]},"is_claimable":false,"name":"Targeting cancer-associated fibroblasts/tumor cells cross-talk inhibits intrahepatic cholangiocarcinoma progression via cell-cycle arrest.","description":"<h4>Background</h4>Cancer-associated fibroblasts (CAFs), mainly responsible for the desmoplastic reaction hallmark of intrahepatic Cholangiocarcinoma (iCCA), likely have a role in tumor aggressiveness and resistance to therapy, although the molecular mechanisms involved are unknown. Aim of the study is to investigate how targeting hCAF/iCCA cross-talk with a Notch1 inhibitor, namely Crenigacestat, may affect cancer progression.<h4>Methods</h4>We used different in vitro models in 2D and established new 3D hetero-spheroids with iCCA cells and human (h)CAFs. The results were confirmed in a xenograft model, and explanted tumoral tissues underwent transcriptomic and bioinformatic analysis.<h4>Results</h4>hCAFs/iCCA cross-talk sustains increased migration of both KKU-M213 and KKU-M156 cells, whi","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-04-30T00:05:56.247Z","creation":"2025-04-06T14:23:23.378Z"},"accession":"S-EPMC11484308","cross_references":{"pubmed":["39415286"],"doi":["10.1186/s13046-024-03210-9"]}}