{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shen C"],"funding":["National Center for Advancing Translational Sciences","American Cancer Society","NCATS NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["gkaf983"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12489472"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["53(18)"],"pubmed_abstract":["KRAS activating mutations occur in 90%-95% of pancreatic adenocarcinoma (PC) and contribute to tumor progression and resistance to therapy, including radiotherapy. A screen in isogenic cells revealed that KRAS activation positively modulates STN1 expression, a component of the CTC1-STN1-TEN1 (CST) complex. We find that STN1 is significantly upregulated in PC and its elevation is correlated with KRAS oncogenic mutations, while inhibition of KRAS signaling decreases STN1 expression. Interestingly, depletion of STN1 increases DNA damage and replication stress, and sensitizes PC cells to ionizing radiation independent of CTC1 and TEN1. STN1 silencing reduces both homologous recombination and non-homologous end joining repair of double-strand breaks (DSBs), suggesting STN1 ensures proper DSB re"],"journal":["Nucleic acids research"],"pubmed_title":["KRAS-induced STN1 (OBFC1) promotes proper CTC1-STN1-TEN1 complex-independent DNA double-strand break repair and cell cycle checkpoint maintenance in pancreatic cancer."],"pmcid":["PMC12489472"],"funding_grant_id":["KL2TR001068","R01 CA198128","P30 CA016058","R01CA246553","RSG-17-221-01-TBG"],"pubmed_authors":["Li H","Yang L","Schaeffer DF","Shen C","Shen B","Cui T","Nair S","Fernandez A","Corrales-Guerrero S","Ping X","Williams TM","Gui L","Renouf DJ","Stark JM","Topham JT","Karasinska JM"],"additional_accession":[]},"is_claimable":false,"name":"KRAS-induced STN1 (OBFC1) promotes proper CTC1-STN1-TEN1 complex-independent DNA double-strand break repair and cell cycle checkpoint maintenance in pancreatic cancer.","description":"KRAS activating mutations occur in 90%-95% of pancreatic adenocarcinoma (PC) and contribute to tumor progression and resistance to therapy, including radiotherapy. A screen in isogenic cells revealed that KRAS activation positively modulates STN1 expression, a component of the CTC1-STN1-TEN1 (CST) complex. We find that STN1 is significantly upregulated in PC and its elevation is correlated with KRAS oncogenic mutations, while inhibition of KRAS signaling decreases STN1 expression. Interestingly, depletion of STN1 increases DNA damage and replication stress, and sensitizes PC cells to ionizing radiation independent of CTC1 and TEN1. STN1 silencing reduces both homologous recombination and non-homologous end joining repair of double-strand breaks (DSBs), suggesting STN1 ensures proper DSB re","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-30T03:31:36.685Z","creation":"2026-06-30T03:24:13.307Z"},"accession":"S-EPMC12489472","cross_references":{"pubmed":["41036624"],"doi":["10.1093/nar/gkaf983"]}}