ArticleCancer science2024
The molecular mechanism underlying KRAS regulation on STK31 expression in pancreatic ductal adenocarcinoma.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Bispecific Antibody and Antibody-Drug Conjugate as Novel Candidates for Treating Pancreatic Ductal Adenocarcinoma.Biomolecules · 2025Review
- Comprehensive Bioinformatics Analyses and Experimental Validation of the Cell Cycle Related Protein SAPCD2 as a New Biomarker and Potential Therapeutic Target in Pancreatic Cancer.Journal of inflammation research · 2025Article
- The molecular mechanism underlying KRAS regulation on STK31 expression in pancreatic ductal adenocarcinoma.Cancer science · 2024Article
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Authors and funding
8 authors.
Funding
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
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