{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T13:02:25Z","timestamp":1790946145655,"version":"4.1.0"},"reference-count":14,"publisher":"S. Karger AG","issue":"5","license":[{"start":{"date-parts":[[2022,1,1]],"date-time":"2022-01-01T00:00:00Z","timestamp":1640995200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2022,1,1]],"date-time":"2022-01-01T00:00:00Z","timestamp":1640995200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Haematol"],"published-print":{"date-parts":[[2022]]},"abstract":"<b><i>Introduction:<\/i><\/b> Chronic myeloid leukaemia (CML) is a myeloproliferative neoplasm characterized by constitutive activity of the tyrosine kinase BCR-ABL1. Drug resistance remains one of the major challenges in CML therapy. MicroRNA (miR)-199a-3p plays an important role in many tumours but has rarely been investigated in CML. We aimed to analyse the role and mechanism of miR-199a-3p in regulating imatinib resistance in CML. <b><i>Methods:<\/i><\/b> The expression of miR-199a-3p and mammalian target of rapamycin (mTOR) in the serum of CML patients and CML cells was examined by quantitative real-time polymerase chain reaction. The levels of apoptosis-related proteins were determined using western blot. The relative cell survival rate and cell proliferation were determined using a CCK-8 assay and a bromodeoxyuridine (BrdU) assay, respectively. Cell cycle and apoptosis were analysed using flow cytometry. Moreover, a dual-luciferase reporter assay was performed to verify the correlation between miR-199a-3p and mTOR. <b><i>Results:<\/i><\/b> MiR-199a-3p was downregulated in the serum of CML patients and in CML cells, while mTOR was upregulated. Both miR-199a-3p overexpression and mTOR silencing inhibited CML cell proliferation, promoted CML cell apoptosis, and sensitized these cells to imatinib. mTOR silencing reversed the promoting effect of miR-199a-3p inhibition on the proliferation of CML cells and the inhibitory effects on cell apoptosis and sensitivity to imatinib. MiR-199a-3p directly targeted mTOR. <b><i>Conclusion:<\/i><\/b> MiR-199a-3p suppressed cell propagation, facilitated apoptosis of CML cells, and sensitized CML cells to imatinib by downregulating mTOR signalling. <\/jats:p>","DOI":"10.1159\/000524158","type":"journal-article","created":{"date-parts":[[2022,3,21]],"date-time":"2022-03-21T22:00:33Z","timestamp":1647900033000},"page":"484-498","source":"Crossref","is-referenced-by-count":7,"title":["MiR-199a-3p Overexpression Suppressed Cell Proliferation and Sensitized Chronic Myeloid Leukaemia Cells to Imatinib by Inhibiting mTOR Signalling"],"prefix":"10.1159","volume":"145","author":[{"given":"Xin","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miao-Miao","family":"Cui","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hai-Zhen","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pei-Yi","family":"Fu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo-Chuan","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2022,3,21]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1038\/243290a0"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1016\/s0140-6736(13)62120-0"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.25011"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1016\/j.leukres.2017.01.005"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1182\/asheducation-2009.1.461"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2016-09-696013"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1016\/j.canlet.2012.03.021"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-017-2485-1"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2020.07.007"},{"key":"ref10","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2018.09.034"},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.26355\/eurrev_202002_20341"},{"key":"ref12","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2009.01.002"},{"key":"ref13","doi-asserted-by":"publisher","DOI":"10.1080\/10428194.2018.1543875"},{"key":"ref14","doi-asserted-by":"publisher","DOI":"10.1007\/s10565-021-09604-1"}],"container-title":["Acta Haematologica"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/524158","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/524158","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T15:58:42Z","timestamp":1745423922000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000524158"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2022]]},"references-count":14,"journal-issue":{"issue":"5","published-online":{"date-parts":[[2022,9,20]]}},"URL":"https:\/\/doi.org\/10.1159\/000524158","archive":["Portico"],"relation":{"is-supplemented-by":[{"id-type":"doi","id":"10.6084\/m9.figshare.19391399","asserted-by":"subject"}]},"ISSN":["0001-5792","1421-9662"],"issn-type":[{"value":"0001-5792","type":"print"},{"value":"1421-9662","type":"electronic"}],"subject":[],"published":{"date-parts":[[2022]]}}}