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Activation of metabolism signaling pathway has been connected with BCR::ABL1-independent TKIs resistance in CML cells. However, the specific mechanism by which metabolism signaling mediates this drug resistance remains unclear. Here, we identified one relationship between glutamine synthetase (GS) and BCR::ABL1-independent Imatinib resistance in CML cells.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>GS and <jats:italic>PXN-AS1<\/jats:italic> in bone marrow samples of CML patients with Imatinib resistance (IR) were screened and detected by whole transcriptome sequencing. GS expression was upregulated using LVs and blocked using shRNAs respectively, then GS expression, Gln content, and cell cycle progression were respectively tested. The CML IR mice model were established by tail vein injection, prognosis of CML IR mice model were evaluated by Kaplan\u2013Meier analysis, the ratio of spleen\/body weight, HE staining, and IHC. <jats:italic>PXN-AS1<\/jats:italic> level was blocked using shRNAs, and the effects of <jats:italic>PXN-AS1<\/jats:italic> on CML IR cells in vitro and in vivo were tested the same as GS. Several RNA-RNA tools were used to predict the potential target microRNAs binding to both GS and <jats:italic>PXN-AS1<\/jats:italic>. RNA mimics and RNA inhibitors were used to explore the mechanism through which <jats:italic>PXN-AS1<\/jats:italic> regulates <jats:italic>miR-635 <\/jats:italic>or<jats:italic> miR-635<\/jats:italic> regulates GS.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>GS was highly expressed in the bone marrow samples of CML patients with Imatinib resistance. In addition, the lncRNA <jats:italic>PXN-AS1<\/jats:italic> was found to mediate GS expression and disorder cell cycle in CML IR cells via mTOR signaling pathway. <jats:italic>PXN-AS1<\/jats:italic> regulated GS expression by binding to <jats:italic>miR-635<\/jats:italic>. Additionally, knockdown of <jats:italic>PXN-AS1<\/jats:italic> attenuated BCR::ABL1-independent Imatinib resistance in CML cells via <jats:italic>PXN-AS1<\/jats:italic>\/<jats:italic>miR-635<\/jats:italic>\/GS\/Gln\/mTOR signaling pathway.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Thus, <jats:italic>PXN-AS1<\/jats:italic> promotes GS-mediated BCR::ABL1-independent Imatinib resistance in CML cells via cell cycle signaling pathway.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Graphic Abstract<\/jats:title>\n                \n              <\/jats:sec>","DOI":"10.1186\/s12935-024-03363-9","type":"journal-article","created":{"date-parts":[[2024,5,29]],"date-time":"2024-05-29T13:02:09Z","timestamp":1716987729000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Long non-coding RNA PXN-AS1 promotes glutamine synthetase-mediated chronic myeloid leukemia BCR::ABL1-independent resistance to Imatinib via cell cycle signaling pathway"],"prefix":"10.1186","volume":"24","author":[{"given":"Yifei","family":"Li","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shiyi","family":"Yuan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ying","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jingwen","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xuan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ping","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wenrui","family":"Xiao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ying","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianchuan","family":"Deng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shifeng","family":"Lou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2024,5,29]]},"reference":[{"issue":"10314","key":"3363_CR1","doi-asserted-by":"publisher","first-page":"1914","DOI":"10.1016\/S0140-6736(21)01204-6","volume":"398","author":"J Cortes","year":"2021","unstructured":"Cortes J, Pavlovsky C, Sau\u00dfele S. 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