<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang J</submitter><funding>The China Medical Association of Minorities Research Project</funding><funding>The Open Fund Project, Associated Key Laboratory of Traditional Mongolia Medicine Research and Development, National Ethnic Affairs Commission and Ministry of Education of China</funding><funding>The China National Traditional Chinese Medicine Inheritance and Innovation Team Sub-Project</funding><funding>The National Natural Science Foundation of China</funding><pagination>2</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11699780</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>With extended gefitinib treatment, the therapeutic effect in some non-small cell lung cancer (NSCLC) patients declined with the development of drug resistance. Aidi injection (ADI) is utilized in various cancers as a traditional Chinese medicine prescription. This study explores the molecular mechanism by which ADI, when combined with gefitinib, attenuates gefitinib resistance in PC9GR NSCLC cells.&lt;h4>Methods&lt;/h4>In vitro and in vivo pharmacological experiments were conducted in PC9GR cells and NSG mice with PC9GR cell-derived tumors, respectively. The molecular mechanism of ADI was further studied using whole-transcriptome sequencing technology. Bioinformatics and molecular biology methods were employed to validate the critical targets of ADI.&lt;h4>Results&lt;/h4>Firstly, AD</pubmed_abstract><journal>Chinese medicine</journal><pubmed_title>Aidi injection inhibits the migration and invasion of gefitinib-resistant lung adenocarcinoma cells by regulating the PLAT/FAK/AKT pathway.</pubmed_title><pmcid>PMC11699780</pmcid><funding_grant_id>MDK2020013</funding_grant_id><funding_grant_id>2020MZ298-110101</funding_grant_id><funding_grant_id>ZYYCXTD-C-202005-10</funding_grant_id><funding_grant_id>82074284</funding_grant_id><pubmed_authors>Zhang F</pubmed_authors><pubmed_authors>Sheng X</pubmed_authors><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Qiao C</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Wu C</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Guo S</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Liu S</pubmed_authors><pubmed_authors>Luo H</pubmed_authors><pubmed_authors>Wang T</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Lu S</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Yang S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Aidi injection inhibits the migration and invasion of gefitinib-resistant lung adenocarcinoma cells by regulating the PLAT/FAK/AKT pathway.</name><description>&lt;h4>Background&lt;/h4>With extended gefitinib treatment, the therapeutic effect in some non-small cell lung cancer (NSCLC) patients declined with the development of drug resistance. Aidi injection (ADI) is utilized in various cancers as a traditional Chinese medicine prescription. This study explores the molecular mechanism by which ADI, when combined with gefitinib, attenuates gefitinib resistance in PC9GR NSCLC cells.&lt;h4>Methods&lt;/h4>In vitro and in vivo pharmacological experiments were conducted in PC9GR cells and NSG mice with PC9GR cell-derived tumors, respectively. The molecular mechanism of ADI was further studied using whole-transcriptome sequencing technology. Bioinformatics and molecular biology methods were employed to validate the critical targets of ADI.&lt;h4>Results&lt;/h4>Firstly, AD</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan</publication><modification>2025-04-03T23:16:48.098Z</modification><creation>2025-04-03T23:16:48.098Z</creation></dates><accession>S-EPMC11699780</accession><cross_references><pubmed>39754146</pubmed><doi>10.1186/s13020-024-01054-1</doi></cross_references></HashMap>