{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T11:03:30Z","timestamp":1791198210811,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2010,1,7]],"date-time":"2010-01-07T00:00:00Z","timestamp":1262822400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2010,4]]},"abstract":"<jats:p>Arsenic trioxide (ATO), an ancient traditional Chinese medicine, has been successfully used as a therapeutic agent for leukemia. Drug resistance and toxicity are major concerns with the treatment. MicroRNAs (miRNAs) are endogenous small non\u2010coding RNA molecules that might modulate cellular sensitivity to anticancer drugs. miRNA\u201021 (miR\u201021) is one of the most prominent miRNAs involved in various aspects of human cancers. However, miR\u201021 has been rarely characterized in chronic myelogenous leukemia (CML). Here, we used a specific anti\u2010miR\u201021 oligonucleotide (AMO\u2010miR\u201021) to sensitize K562 cells to ATO by degradation of miR\u201021. The results showed that both AMO\u2010miR\u201021 and ATO caused growth inhibition, apoptosis, and G1\u2010phase arrest in K562 cells. Meanwhile, AMO\u2010miR\u201021 significantly promoted ATO\u2010mediated growth inhibition and apotosis without affecting the G1 phase. Apoptotic cells were confirmed morphologically with Giemsa\u2019s staining. Furthermore, dual\u2010luciferase reporter vector, containing two tandem miR\u201021 binding sites from PDCD4 3\u2032UTR, validated that PDCD4 was directly regulated by miR\u201021. Therefore, AMO\u2010miR\u201021 sensitized leukemic K562 cells to ATO by inducing apoptosis partially due to its up\u2010regulation of PDCD4 protein level. The combination of ATO and AMO\u2010miR\u201021 present therapeutic potential for CML.<\/jats:p><jats:p>(<jats:italic>Cancer Sci<\/jats:italic> 2010; 101: 948\u2013954)<\/jats:p>","DOI":"10.1111\/j.1349-7006.2010.01489.x","type":"journal-article","created":{"date-parts":[[2010,1,7]],"date-time":"2010-01-07T14:01:07Z","timestamp":1262872867000},"page":"948-954","source":"Crossref","is-referenced-by-count":66,"title":["Anti\u2010miR\u201021 oligonucleotide sensitizes leukemic K562 cells to arsenic trioxide by inducing 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