<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen Y</submitter><funding>Guangxi Medical University Undergraduate Education and Teaching Reform Project</funding><funding>Natural Science Foundation of Guangxi Province</funding><funding>Future Academic Star of Guangxi Medical University</funding><funding>China Undergraduate Innovation and Entrepreneurship Training Program</funding><funding>Guangxi Higher Education Undergraduate Teaching Reform Project</funding><funding>Guangxi Zhuang Autonomous Region Administration of Traditional Chinese Medicine Scientific Research Project</funding><funding>Guangxi Educational Science Planning Key Project</funding><pagination>e70017</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12041129</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(1)</volume><pubmed_abstract>SAE1, a key factor in tumour development, has not been thoroughly examined in pancreatic adenocarcinoma (PAAD), a cancer with high incidence and poor prognosis. We conducted a comprehensive study, integrating mRNA data, immunohistochemistry, CRISPR-modified cell line analysis and single-cell RNA sequencing to assess SAE1's role in PAAD. We also used ChIP-Seq to explore SAE1's transcriptional regulation and analysed clinical data, drug sensitivity and molecular docking models. SAE1 mRNA was significantly overexpressed in PAAD, with a substantial impact on cell proliferation and migration. Functional analyses linked SAE1 to cell cycle and DNA replication pathways, suggesting a role in PAAD development. Our study indicates that SAE1 may promote PAAD through cell cycle pathways, with FOXA1 pot</pubmed_abstract><journal>IET systems biology</journal><pubmed_title>SAE1 May Play a Pro-Carcinogenic Role in Pancreatic Adenocarcinoma: A Comprehensive Study Integrating Multiple Pieces of Evidence.</pubmed_title><pmcid>PMC12041129</pmcid><funding_grant_id>2022JGA146</funding_grant_id><funding_grant_id>S202410598212</funding_grant_id><funding_grant_id>2023Z10</funding_grant_id><funding_grant_id>2022ZJY2791</funding_grant_id><funding_grant_id>GXZYA20230267</funding_grant_id><funding_grant_id>2025GXNSFAA069660</funding_grant_id><funding_grant_id>WLXSZX24118</funding_grant_id><funding_grant_id>GXZYA20230270</funding_grant_id><pubmed_authors>Yu N</pubmed_authors><pubmed_authors>Chen G</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Li SD</pubmed_authors><pubmed_authors>Chi BT</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Wu T</pubmed_authors><pubmed_authors>Meng LJ</pubmed_authors><pubmed_authors>Wei DM</pubmed_authors><pubmed_authors>Li MJ</pubmed_authors><pubmed_authors>Chen XJ</pubmed_authors><pubmed_authors>Huang SN</pubmed_authors><pubmed_authors>Ye YP</pubmed_authors></additional><is_claimable>false</is_claimable><name>SAE1 May Play a Pro-Carcinogenic Role in Pancreatic Adenocarcinoma: A Comprehensive Study Integrating Multiple Pieces of Evidence.</name><description>SAE1, a key factor in tumour development, has not been thoroughly examined in pancreatic adenocarcinoma (PAAD), a cancer with high incidence and poor prognosis. We conducted a comprehensive study, integrating mRNA data, immunohistochemistry, CRISPR-modified cell line analysis and single-cell RNA sequencing to assess SAE1's role in PAAD. We also used ChIP-Seq to explore SAE1's transcriptional regulation and analysed clinical data, drug sensitivity and molecular docking models. SAE1 mRNA was significantly overexpressed in PAAD, with a substantial impact on cell proliferation and migration. Functional analyses linked SAE1 to cell cycle and DNA replication pathways, suggesting a role in PAAD development. Our study indicates that SAE1 may promote PAAD through cell cycle pathways, with FOXA1 pot</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan-Dec</publication><modification>2025-06-25T03:06:03.297Z</modification><creation>2025-06-25T03:06:03.297Z</creation></dates><accession>S-EPMC12041129</accession><cross_references><pubmed>40302186</pubmed><doi>10.1049/syb2.70017</doi></cross_references></HashMap>