{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T13:11:15Z","timestamp":1788527475969,"version":"build-2803163510"},"reference-count":80,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T00:00:00Z","timestamp":1770940800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      (\n                      <jats:italic>H. pylori<\/jats:italic>\n                      ), a spiral Gram-negative bacterium colonizing gastric mucosa, damages epithelial cells, driving chronic gastritis, peptic ulcers, and gastric cancer. Mechanisms of its malignant transformation remain unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We identified differentially expressed genes (DEGs) and hub genes, pathway enrichment analysis, transcription factors (TFs), small-molecule drug and molecular docking prediction using gastric epithelial cells (GECs) infected with\n                      <jats:italic>H. pylori<\/jats:italic>\n                      strain 26695 and clinical sample datasets.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>H. pylori<\/jats:italic>\n                      infection of GECs, multiple signaling pathways were activated, including the p53, MAPK, TNF, IL-17, PI3K-Akt and NF-\u03baB signaling, DNA replication, Apoptosis, Cell cycle, Necroptosis. A total of 107 co-expressed DEGs were identified\n                      <jats:italic>in vitro<\/jats:italic>\n                      and\n                      <jats:italic>in vivo<\/jats:italic>\n                      . Using Cytoscape, 20 hub genes were prioritized: TNF, CXCL8, NFKBIA, IRF1, ICAM1, TNFAIP3, BIRC3, CXCL1, ITGAM, RELB, CXCL2, CCL20, NFKB2, EGR1, CDKN1A, IRAK2, JAK1, NFKBIE, TRAF1, and JUNB. These hub genes were enriched in NF-\u03baB, TNF and IL-17 signaling, and responses to bacterial pathogens or lipopolysaccharide. Further analysis identified 9 upregulated TFs: VDR, SPI1, ETS2, STAT1, E2F1, PML, ETS1, BRCA1, MYC, and 4 downregulated TFs: ING4, CEBPD, HSF1, JUN. To explore potential therapeutic interventions, we performed small-molecule drug prediction and molecular docking for hub genes revealed: Simvastatin: Linked to CCL20, NFKBIA, and ICAM1. Atorvastatin: Associated with CDKN1A, ICAM1, and TNF. TPCA-1: Targeting JAK1.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      These findings provide a theoretical foundation for further investigation into the molecular mechanisms underlying\n                      <jats:italic>H. pylori<\/jats:italic>\n                      -related diseases.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcimb.2026.1688009","type":"journal-article","created":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T05:22:15Z","timestamp":1770960135000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Integrated transcriptomics and molecular docking identify hub genes and statin regulators in Helicobacter pylori-associated gastric mucosal pathogenesis"],"prefix":"10.3389","volume":"16","author":[{"given":"Minglin","family":"Zhang","sequence":"first","affiliation":[{"name":"Health Management Medicine Center, The Third Xiangya Hospital, Central South University","place":["Changsha, Hunan, China"]},{"name":"Department of Gastroenterology, The Third Xiangya Hospital, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xue","family":"He","sequence":"additional","affiliation":[{"name":"Health Management Medicine Center, The Third Xiangya Hospital, Central South University","place":["Changsha, Hunan, China"]},{"name":"Nursing Department, The Third Xiangya Hospital, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuelin","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Third Xiangya Hospital, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ting","family":"Cai","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Hunan Provincial People\u2019s Hospital, The First Affiliated Hospital of Hunan Normal University","place":["Changsha, Hunan, China"]},{"name":"Hunan Provincial University Key Laboratory of the Fundamental and Clinical Research on Functional Nucleic Acid, Changsha Medical University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoming","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Third Xiangya Hospital, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fen","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Third Xiangya Hospital, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,2,13]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"8099","DOI":"10.4049\/jimmunol.0900664","article-title":"Helicobacter pylori induces MAPK phosphorylation and AP-1 activation via a NOD1-dependent mechanism","volume":"183","author":"Allison","year":"2009","journal-title":"J. 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