<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>112(2)</volume><submitter>You R</submitter><pubmed_abstract>The stromal niche plays a pivotal role in AML chemoresistance and energy metabolism reprogramming is a hallmark of a tumor. 5'-Adenosine monophosphate-activated protein kinase (AMPK) is an important energy sensor suppressing mammalian target of rapamycin complex 1 (mTORC1) activity. However, the role of AMPK-mTORC1 pathway on connecting AML cell energy metabolism reprogramming and chemoresistance induced by the bone marrow microenvironment (BMM) is not defined. Here, with a co-culture system that simulates the interaction between BMM and AML cells, it is shown that stromal contact led to a decreased sensitivity to chemotherapy accompanied by an increase of oxidative phosphorylation (OXPHOS) activity and mitochondrial ATP synthesis in AML cells. The increased OXPHOS activity and excessive A</pubmed_abstract><journal>Journal of leukocyte biology</journal><pagination>299-311</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9544716</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Bone marrow microenvironment drives AML cell OXPHOS addiction and AMPK inhibition to resist chemotherapy.</pubmed_title><pmcid>PMC9544716</pmcid><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Pan Z</pubmed_authors><pubmed_authors>Chen P</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Li D</pubmed_authors><pubmed_authors>Feng X</pubmed_authors><pubmed_authors>Huang H</pubmed_authors><pubmed_authors>Hou D</pubmed_authors><pubmed_authors>You R</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Kang L</pubmed_authors><pubmed_authors>Xiao Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bone marrow microenvironment drives AML cell OXPHOS addiction and AMPK inhibition to resist chemotherapy.</name><description>The stromal niche plays a pivotal role in AML chemoresistance and energy metabolism reprogramming is a hallmark of a tumor. 5'-Adenosine monophosphate-activated protein kinase (AMPK) is an important energy sensor suppressing mammalian target of rapamycin complex 1 (mTORC1) activity. However, the role of AMPK-mTORC1 pathway on connecting AML cell energy metabolism reprogramming and chemoresistance induced by the bone marrow microenvironment (BMM) is not defined. Here, with a co-culture system that simulates the interaction between BMM and AML cells, it is shown that stromal contact led to a decreased sensitivity to chemotherapy accompanied by an increase of oxidative phosphorylation (OXPHOS) activity and mitochondrial ATP synthesis in AML cells. The increased OXPHOS activity and excessive A</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2025-04-22T02:01:16.341Z</modification><creation>2025-04-05T20:11:53.966Z</creation></dates><accession>S-EPMC9544716</accession><cross_references><pubmed>34927743</pubmed><doi>10.1002/JLB.6A0821-409RR</doi></cross_references></HashMap>