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The molecular regulators of lineage choices in the context of tyrosine kinase inhibitor (TKI) resistance remain poorly understood in chronic myeloid leukemia (CML). To find a potential molecular regulator contributing to lineage distribution and TKI resistance, we undertook an RNA-sequencing approach for identifying microRNAs (miRNAs). Following an unbiased screen, elevated miRNA182-5p levels were detected in Bcr-Abl-inhibited K562 cells (CML blast crisis cell line) and in a panel of CML patients. Earlier, miRNA182-5p upregulation was reported in several solid tumours and haematological malignancies. We undertook a strategy involving transient modulation and CRISPR\/Cas9 (clustered regularly interspersed short palindromic repeats)-mediated knockout of the <jats:italic>MIR182<\/jats:italic> locus in CML cells. The lineage contribution was assessed by methylcellulose colony formation assay. The transient modulation of miRNA182-5p revealed a biased phenotype. Strikingly, <jats:italic>\u0394182<\/jats:italic> cells (homozygous deletion of <jats:italic>MIR182<\/jats:italic> locus) produced a marked shift in lineage distribution. The phenotype was rescued by ectopic expression of miRNA182-5p in <jats:italic>\u0394182<\/jats:italic> cells. A bioinformatic analysis and Hes1 modulation data suggested that Hes1 could be a putative target of miRNA182-5p. A reciprocal relationship between miRNA182-5p and Hes1 was seen in the context of TK inhibition. In conclusion, we reveal a key role for miRNA182-5p in restricting the myeloid development of leukemic cells. We propose that the <jats:italic>\u0394182<\/jats:italic> cell line will be valuable in designing experiments for next-generation pharmacological interventions.<\/jats:p>","DOI":"10.1038\/cddis.2016.471","type":"journal-article","created":{"date-parts":[[2017,1,12]],"date-time":"2017-01-12T13:47:21Z","timestamp":1484228841000},"page":"e2547-e2547","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["MiRNA182 regulates percentage of myeloid and erythroid cells in chronic myeloid leukemia"],"prefix":"10.1038","volume":"8","author":[{"given":"Deepak","family":"Arya","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sasikala P","family":"Sachithanandan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cecil","family":"Ross","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dasaradhi","family":"Palakodeti","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shang","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sudhir","family":"Krishna","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2017,1,12]]},"reference":[{"key":"BFcddis2016471_CR1","doi-asserted-by":"publisher","first-page":"215","DOI":"10.1016\/j.it.2012.01.012","volume":"33","author":"G Costa","year":"2012","unstructured":"Costa G, Kouskoff V, Lacaud G . 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