{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu Y"],"funding":["National Natural Science Foundation of China","the General Research Fund, Research Grants Council of Hong Kong"],"pagination":["3288-3304"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11447899"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["115(10)"],"pubmed_abstract":["KRAS gene mutations are common in pancreatic ductal adenocarcinoma (PDAC), but targeting mutant KRAS is still challenging. Here, an endoribonuclease-prepared small interfering RNA (esiRNA) library was used to screen new kinases that play critical roles in PDAC driven by KRAS gene mutations, and serine/threonine kinase 31 (STK31) was identified and characterized as a potential therapeutic target for KRAS-mutant PDAC. Our results showed that STK31 was upregulated in KRAS-mutant PDAC patients with poor survival and highly expressed in PDAC cell lines with KRAS<sup>G12D</sup> mutation. Inhibition of STK31 in KRAS-mutant cell lines significantly reduced PDAC cell growth in vitro and hindered tumor growth in vivo. Gain and loss of function experiments revealed that STK31 is a downstream target o"],"journal":["Cancer science"],"pubmed_title":["The molecular mechanism underlying KRAS regulation on STK31 expression in pancreatic ductal adenocarcinoma."],"pmcid":["PMC11447899"],"funding_grant_id":["CUHK14120419","32270618","CUHK14120618","CUHK14171217"],"pubmed_authors":["Liu Y","Wong CH","To KF","Tang SC","Chan SL","Li CH","Chen Y","Li B"],"additional_accession":[]},"is_claimable":false,"name":"The molecular mechanism underlying KRAS regulation on STK31 expression in pancreatic ductal adenocarcinoma.","description":"KRAS gene mutations are common in pancreatic ductal adenocarcinoma (PDAC), but targeting mutant KRAS is still challenging. Here, an endoribonuclease-prepared small interfering RNA (esiRNA) library was used to screen new kinases that play critical roles in PDAC driven by KRAS gene mutations, and serine/threonine kinase 31 (STK31) was identified and characterized as a potential therapeutic target for KRAS-mutant PDAC. Our results showed that STK31 was upregulated in KRAS-mutant PDAC patients with poor survival and highly expressed in PDAC cell lines with KRAS<sup>G12D</sup> mutation. Inhibition of STK31 in KRAS-mutant cell lines significantly reduced PDAC cell growth in vitro and hindered tumor growth in vivo. Gain and loss of function experiments revealed that STK31 is a downstream target o","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2025-04-05T08:57:37.079Z","creation":"2025-04-05T08:57:37.079Z"},"accession":"S-EPMC11447899","cross_references":{"pubmed":["39054797"],"doi":["10.1111/cas.16286"]}}