<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dong L</submitter><funding>China Medicine Education Association 2024 Annual Medicine Science and Technology Tackling Projects</funding><funding>The National Administration of Traditional Chinese Medicine Talent Exchange Center - Independent Project of the Collaborative Innovation and Transformation Project for High Quality Development of Traditional Chinese Medicine</funding><funding>Traditional Chinese Medicine Scientific Research Project of of Henan Province</funding><pagination>2184</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12662956</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>Colorectal cancer (CRC) represented a pervasive manifestation of malignant neoplasia within the digestive tract. Apigenin, exhibiting a multitude of physiological attributes and pharmacological actions, has undergone extensive scrutiny for its antitumor efficacy and benign toxicity profile. Cisplatin (DDP)-centered chemotherapy constituted a pivotal aspect of multidisciplinary therapeutic strategies. Nevertheless, resistance to DDP posed a considerable impediment to the efficacy of CRC chemotherapy. The aim of this investigation was to assess the impact of combining Apigenin with DDP on the proliferation and apoptotic processes of human CRC cells, while also delving into the underlying mechanisms. HCT116 and SW480 were cultivated and subjected to treatment with Apigenin (API) either as a m</pubmed_abstract><journal>Discover oncology</journal><pubmed_title>Apigenin combined with cisplatin suppressed the progression of colorectal cancer by targeting the KRT23/Wnt/β-catenin signaling pathway.</pubmed_title><pmcid>PMC12662956</pmcid><funding_grant_id>CXZH202303</funding_grant_id><funding_grant_id>2023ZY1027</funding_grant_id><funding_grant_id>2025ZY3115</funding_grant_id><funding_grant_id>2024ZY3107</funding_grant_id><funding_grant_id>2024KTM019</funding_grant_id><pubmed_authors>Si L</pubmed_authors><pubmed_authors>Jiao P</pubmed_authors><pubmed_authors>Huang M</pubmed_authors><pubmed_authors>Dong L</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Guo Q</pubmed_authors><pubmed_authors>Gong Y</pubmed_authors><pubmed_authors>Yang F</pubmed_authors><pubmed_authors>Song J</pubmed_authors><pubmed_authors>Zhang W</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Luo L</pubmed_authors><pubmed_authors>Kang M</pubmed_authors><pubmed_authors>Wang X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Apigenin combined with cisplatin suppressed the progression of colorectal cancer by targeting the KRT23/Wnt/β-catenin signaling pathway.</name><description>Colorectal cancer (CRC) represented a pervasive manifestation of malignant neoplasia within the digestive tract. Apigenin, exhibiting a multitude of physiological attributes and pharmacological actions, has undergone extensive scrutiny for its antitumor efficacy and benign toxicity profile. Cisplatin (DDP)-centered chemotherapy constituted a pivotal aspect of multidisciplinary therapeutic strategies. Nevertheless, resistance to DDP posed a considerable impediment to the efficacy of CRC chemotherapy. The aim of this investigation was to assess the impact of combining Apigenin with DDP on the proliferation and apoptotic processes of human CRC cells, while also delving into the underlying mechanisms. HCT116 and SW480 were cultivated and subjected to treatment with Apigenin (API) either as a m</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Nov</publication><modification>2026-06-08T03:17:06.726Z</modification><creation>2026-06-08T03:08:36.561Z</creation></dates><accession>S-EPMC12662956</accession><cross_references><pubmed>41313558</pubmed><doi>10.1007/s12672-025-03942-w</doi></cross_references></HashMap>