<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>21(5)</volume><submitter>Wang Z</submitter><pubmed_abstract>Understanding the specific role and underlying mechanisms of mitophagy may provide therapeutic benefit to patients with nasopharyngeal carcinoma (NPC). Forkhead box D1 (&lt;i>FOXD1&lt;/i>), is overexpressed in NPC. However, its roles in NPC progression and therapy resistance remain largely unknown. NPC tissues displayed increased &lt;i>FOXD1&lt;/i> expression compared to paired non-tumor tissues, which correlated with worse overall survival (OS). Upregulation of &lt;i>FOXD1&lt;/i> promoted NPC cell proliferation, colony formation, migration, invasion, and impaired sensitivity to GEM by enhancing mitophagy levels. Mechanistically, &lt;i>FOXD1&lt;/i> promoted mitophagy in NPC cells by transcriptionally initiating BNIP3 expression. This enhanced mitophagy, in turn, promoted proliferation, invasion, and migration and</pubmed_abstract><journal>International journal of biological sciences</journal><pagination>1894-1913</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11900802</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Targeting ALG3/FOXD1/BNIP3 Axis Prevents Mitophagy and Gemcitabine Resistance of Nasopharyngeal Carcinoma.</pubmed_title><pmcid>PMC11900802</pmcid><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Cao K</pubmed_authors><pubmed_authors>He D</pubmed_authors><pubmed_authors>Xiao M</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Jin Y</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Cheng Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting ALG3/FOXD1/BNIP3 Axis Prevents Mitophagy and Gemcitabine Resistance of Nasopharyngeal Carcinoma.</name><description>Understanding the specific role and underlying mechanisms of mitophagy may provide therapeutic benefit to patients with nasopharyngeal carcinoma (NPC). Forkhead box D1 (&lt;i>FOXD1&lt;/i>), is overexpressed in NPC. However, its roles in NPC progression and therapy resistance remain largely unknown. NPC tissues displayed increased &lt;i>FOXD1&lt;/i> expression compared to paired non-tumor tissues, which correlated with worse overall survival (OS). Upregulation of &lt;i>FOXD1&lt;/i> promoted NPC cell proliferation, colony formation, migration, invasion, and impaired sensitivity to GEM by enhancing mitophagy levels. Mechanistically, &lt;i>FOXD1&lt;/i> promoted mitophagy in NPC cells by transcriptionally initiating BNIP3 expression. This enhanced mitophagy, in turn, promoted proliferation, invasion, and migration and</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-04-08T19:48:54.685Z</modification><creation>2025-04-04T09:07:47.68Z</creation></dates><accession>S-EPMC11900802</accession><cross_references><pubmed>40083705</pubmed><doi>10.7150/ijbs.101585</doi></cross_references></HashMap>