{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T02:24:26Z","timestamp":1785896666622,"version":"3.56.0"},"reference-count":31,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,5,30]],"date-time":"2022-05-30T00:00:00Z","timestamp":1653868800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003453","name":"Natural Science Foundation of Guangdong Province","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003453","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:p>In clinical practice, arsenic trioxide can be used to treat a subset of R\/R CML patients, but resistance tends to reappear quickly. We designed an experiment to study arsenic trioxide resistance in K-562 cells. Previously, we identified the <jats:italic>UNC13B<\/jats:italic> gene as potentially responsible for arsenic trioxide resistance in K-562 cells <jats:italic>via<\/jats:italic> gene chip screening followed by high-content screening. We aimed to investigate the role and mechanism of the <jats:italic>UNC13B<\/jats:italic> gene in K-562 cells, an arsenic trioxide-resistant chronic myeloid leukemia cell line. <jats:italic>In vitro<\/jats:italic> lentiviral vector-mediated <jats:italic>UNC13B<\/jats:italic> siRNA transfection was performed on K-562 cells. The roles of <jats:italic>UNC13B<\/jats:italic> in cell proliferation, apoptosis and cell cycle pathways, and colony formation were analyzed by CCK-8 assay, fluorescence-activated cell sorting, and soft agar culture, respectively. Gene chip screening was used to define the possible downstream pathways of <jats:italic>UNC13B<\/jats:italic>. Western blot was performed to further validate the possible genes mediated by <jats:italic>UNC13B<\/jats:italic> for arsenic trioxide resistance in patients with chronic myeloid leukemia. <jats:italic>UNC13B<\/jats:italic> downregulation significantly inhibited growth, promoted apoptosis, decreased colony formation, reduced the duration of the G1 phase, and increased the duration of the S phase of K-562 cells. Western blot results confirmed that <jats:italic>UNC13B<\/jats:italic> may modulate the apoptosis and proliferation of arsenic trioxide-resistant chronic myeloid leukemia cells through the mediation of MAP3K7, CDK4, and PINK1. <jats:italic>UNC13B<\/jats:italic> is a potential therapeutic target for patients with arsenic trioxide-resistant chronic myeloid leukemia.<\/jats:p>","DOI":"10.3389\/fonc.2022.920999","type":"journal-article","created":{"date-parts":[[2022,5,30]],"date-time":"2022-05-30T12:54:04Z","timestamp":1653915244000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["UNC13B Promote Arsenic Trioxide Resistance in Chronic Lymphoid Leukemia Through Mitochondria Quality 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