<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16</volume><submitter>Wu M</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide. Cardamonin (CDN), a bioactive flavonoid derived from the seeds of &lt;i>Alpinia katsumadai&lt;/i> Hayata, has demonstrated broad-spectrum anticancer potential. However, its specific mechanisms and therapeutic targets in CRC remain poorly elucidated.&lt;h4>Methods&lt;/h4>Network pharmacology and molecular docking were employed to identify signaling pathways and targets associated with the anti-CRC activity of CDN. Cell viability, proliferation, migration, and invasion were evaluated using CCK-8, EdU, wound healing, and Transwell assays, respectively. Apoptosis and cell cycle were analyzed by flow cytometry. Proteomic profiling was applied to explore the underlying mechanisms, and the </pubmed_abstract><journal>Frontiers in pharmacology</journal><pagination>1739201</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12823903</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Cardamonin induces apoptosis of colorectal cancer cells via targeted inhibition of the JAK/STAT3/epithelial-mesenchymal transition (EMT) signaling axis.</pubmed_title><pmcid>PMC12823903</pmcid><pubmed_authors>Wu M</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Du Z</pubmed_authors><pubmed_authors>Chen C</pubmed_authors><pubmed_authors>Ren D</pubmed_authors><pubmed_authors>Liu W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cardamonin induces apoptosis of colorectal cancer cells via targeted inhibition of the JAK/STAT3/epithelial-mesenchymal transition (EMT) signaling axis.</name><description>&lt;h4>Background&lt;/h4>Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide. Cardamonin (CDN), a bioactive flavonoid derived from the seeds of &lt;i>Alpinia katsumadai&lt;/i> Hayata, has demonstrated broad-spectrum anticancer potential. However, its specific mechanisms and therapeutic targets in CRC remain poorly elucidated.&lt;h4>Methods&lt;/h4>Network pharmacology and molecular docking were employed to identify signaling pathways and targets associated with the anti-CRC activity of CDN. Cell viability, proliferation, migration, and invasion were evaluated using CCK-8, EdU, wound healing, and Transwell assays, respectively. Apoptosis and cell cycle were analyzed by flow cytometry. Proteomic profiling was applied to explore the underlying mechanisms, and the </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-21T03:10:24.837Z</modification><creation>2026-06-21T03:07:35.581Z</creation></dates><accession>S-EPMC12823903</accession><cross_references><pubmed>41585878</pubmed><doi>10.3389/fphar.2025.1739201</doi></cross_references></HashMap>