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Original Article: Research

MicroRNA-221 sensitizes chronic myeloid leukemia cells to imatinib by targeting STAT5

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Pages 1709-1720 | Received 06 Jun 2018, Accepted 30 Oct 2018, Published online: 05 Dec 2018

References

  • Branford S, Yeung DT, Parker WT, et al. Prognosis for patients with CML and >10% BCR-ABL1 after 3 months of imatinib depends on the rate of BCR-ABL1 decline. Blood. 2014;124:511–518.
  • Huang N, Huang Z, Gao M, et al. Induction of apoptosis in imatinib sensitive and resistant chronic myeloid leukemia cells by efficient disruption of bcr-abl oncogene with zinc finger nucleases. J Exp Clin Cancer Res. 2018;37:62–75.
  • Dalgic CT, Kaymaz BT, Ozkan MC, et al. Investigating the role of JAK/STAT pathway on dasatinib-induced apoptosis for CML cell model K562. Clin Lymphoma Myeloma Leuk. 2015;15:S161–S166.
  • Kantarjian H, O'Brien S, Jabbour E, et al. Improved survival in chronic myeloid leukemia since the introduction of imatinib therapy: a single-institution historical experience. Blood. 2012;119:1981–1987.
  • Massimino M, Stella S, Tirro E, et al. Non ABL-directed inhibitors as alternative treatment strategies for chronic myeloid leukemia. Mol Cancer. 2018;17:56.
  • Hughes TP, Ross DM. Moving treatment-free remission into mainstream clinical practice in CML. Blood. 2016;128:17–23.
  • Jain P, Kantarjian H, Patel KP, et al. Impact of BCR-ABL transcript type on outcome in patients with chronic-phase CML treated with tyrosine kinase inhibitors. Blood. 2016;127:1269–1275.
  • Wang D, Zheng Y, Li J, et al. SHC004-221A1, a novel tyrosine kinase, potently inhibits T315I mutant BCR-ABL in chronic myeloid leukemia. Eur J Pharmacol. 2017;811:117–124.
  • Sillaber C, Gesbert F, Frank DA, et al. STAT5 activation contributes to growth and viability in Bcr/Abl-transformed cells. Blood. 2000;95:2118–2125.
  • Weber A, Borghouts C, Brendel C, et al. Stat5 exerts distinct, vital functions in the cytoplasm and nucleus of Bcr-Abl + K562 and Jak2(V617F)+HEL leukemia cells. Cancers (Basel). 2015;7:503–537.
  • Nieborowska-Skorska M, Wasik MA, Slupianek A, et al. Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis. J Exp Med. 1999;189:1229–1242.
  • Bourgeais J, Ishac N, Medrzycki M, et al. Oncogenic STAT5 signaling promotes oxidative stress in chronic myeloid leukemia cells by repressing antioxidant defenses. Oncotarget. 2017;8:41876–41889.
  • Warsch W, Grundschober E, Berger A, et al. STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia. Oncotarget. 2012;3:1669–1687.
  • Gleixner KV, Schneeweiss M, Eisenwort G, et al. Combined targeting of STAT3 and STAT5: a novel approach to overcome drug resistance in chronic myeloid leukemia. Haematologica. 2017;102:1519–1529.
  • Juen L, Brachet-Botineau M, Parmenon C, et al. New inhibitor targeting signal transducer and activator of transcription 5 (STAT5) signaling in myeloid leukemias. J Med Chem. 2017;60:6119–6136.
  • Tonouchi E, Gen Y, Muramatsu T, et al. miR-3140 suppresses tumor cell growth by targeting BRD4 via its coding sequence and downregulates the BRD4-NUT fusion oncoprotein. Sci Rep. 2018;8:4482.
  • Soltani I, Douzi K, Gharbi H, et al. Downregulation of miR-451 in Tunisian chronic myeloid leukemia patients: potential implication in imatinib resistance. Hematology. 2017;22:201–207.
  • Zhao L, Shan Y, Liu B, et al. Functional screen analysis reveals miR-3142 as central regulator in chemoresistance and proliferation through activation of the PTEN-AKT pathway in CML. Cell Death Dis. 2017;8:e2830.
  • Zhou M, Zeng J, Wang X, et al. MiR-370 sensitizes chronic myeloid leukemia K562 cells to homoharringtonine by targeting Forkhead box M1. J Transl Med. 2013;11:265.
  • Machova Polakova K, Lopotova T, Klamova H, et al. Expression patterns of microRNAs associated with CML phases and their disease related targets. Mol Cancer. 2011;10:41–53.
  • Ihle MA, Trautmann M, Kuenstlinger H, et al. miRNA-221 and miRNA-222 induce apoptosis via the KIT/AKT signalling pathway in gastrointestinal stromal tumours. Mol Oncol. 2015;9:1421–1433.
  • Dentelli P, Traversa M, Rosso A, et al. miR-221/222 control luminal breast cancer tumor progression by regulating different targets. Cell Cycle. 2014;13:1811–1826.
  • Chinese Society of Hematology CMA. The guidelines for diagnosis and treatment of chronic myelogenous leukemia in China (2016 edition). Zhonghua Xue Ye Xue Za Zhi. 2016;37:633–639.
  • Cortes J, Hochhaus A, Hughes T, et al. Front-line and salvage therapies with tyrosine kinase inhibitors and other treatments in chronic myeloid leukemia. JCO. 2011;29:524–531.
  • Chomel JC, Bonnet ML, Sorel N, et al. Leukemic stem cell persistence in chronic myeloid leukemia patients with sustained undetectable molecular residual disease. Blood. 2011;118:3657–3660.
  • Sintim HO, Larocque E, Naganna N, et al. Alkynylnicotinamide-based compounds as ABL1 inhibitors with potent activities against drug-resistant CML harboring ABL1(T315I) mutant kinase. ChemMedChem. 2018;13:1172–1180.
  • Liu C, Nie D, Li J, et al. Antitumor effects of blocking protein neddylation in T315I-BCR-ABL leukemia cells and leukemia stem cells. Cancer Res. 2018;78:1522–1536.
  • Ernst T, La Rosee P, Muller MC, et al. BCR-ABL mutations in chronic myeloid leukemia. Hematol Oncol Clin North Am. 2011;25:997–1008.
  • Rossetti S, Anauo MJ, Sacchi N. MiR-221-regulated KIT level by wild type or leukemia mutant RUNX1: a determinant of single myeloblast fate decisions that - collectively - drives or hinders granulopoiesis. Oncotarget. 2017;8:85783–85793.
  • Rommer A, Steinleitner K, Hackl H, et al. Overexpression of primary microRNA 221/222 in acute myeloid leukemia. BMC Cancer. 2013;13:364.
  • Kotani A, Ha D, Hsieh J, et al. miR-128b is a potent glucocorticoid sensitizer in MLL-AF4 acute lymphocytic leukemia cells and exerts cooperative effects with miR-221. Blood. 2009;114:4169–4178.
  • Okamoto K, Miyoshi K, Murawaki Y. miR-29b, miR-205 and miR-221 enhance chemosensitivity to gemcitabine in HuH28 human cholangiocarcinoma cells. PLoS One. 2013;8:e77623.
  • Liu H, Chang JK, Hou JQ, et al. Inhibition of miR-221 influences bladder cancer cell proliferation and apoptosis. Eur Rev Med Pharmacol Sci. 2017;21:3193–3199.
  • Su M, Wang J, Wang C, et al. MicroRNA-221 inhibits autophagy and promotes heart failure by modulating the p27/CDK2/mTOR axis. Cell Death Differ. 2015;22:986–999.
  • Wu CW, Cheng YW, Hsu NY, et al. MiRNA-221 negatively regulated downstream p27Kip1 gene expression involvement in pterygium pathogenesis. Mol Vis. 2014;20:1048–1056.
  • Stella S, Tirro E, Conte E, et al. Suppression of survivin induced by a BCR-ABL/JAK2/STAT3 pathway sensitizes imatinib-resistant CML cells to different cytotoxic drugs. Mol Cancer Ther. 2013;12:1085–1098.
  • Cheng Y, Hao Y, Zhang A, et al. Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib. Int J Mol Med. 2018;41:455–463.
  • Warsch W, Grundschober E, Sexl V. Adding a new facet to STAT5 in CML: multitasking for leukemic cells. Cell Cycle. 2013;12:1813–1814.
  • Warsch W, Kollmann K, Eckelhart E, et al. High STAT5 levels mediate imatinib resistance and indicate disease progression in chronic myeloid leukemia. Blood. 2011;117:3409–3420.
  • Kosova B, Tezcanli B, Ekiz HA, et al. Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells. Leuk Lymphoma. 2010;51:1895–1901.
  • Rondanin R, Simoni D, Maccesi M, et al. Effects of pimozide derivatives on pSTAT5 in K562 cells. ChemMedChem. 2017;12:1183–1190.
  • Cholez E, Debuysscher V, Bourgeais J, et al. Evidence for a protective role of the STAT5 transcription factor against oxidative stress in human leukemic pre-B cells. Leukemia. 2012;26:2390–2397.
  • Wingelhofer B, Maurer B, Heyes EC, et al. Pharmacologic inhibition of STAT5 in acute myeloid leukemia. Leukemia. 2018;32:1135–1146.
  • Sun T, Jia Y, Xiao D. Interference of STAT 5b expression enhances the chemo-sensitivity of gastric cancer cells to gefitinib by promoting mitochondrial pathway-mediated cell apoptosis. Oncol Rep. 2015;34:227–234.
  • He C, Li L, Guan X, et al. Mutant p53 gain of function and chemoresistance: the role of mutant p53 in response to clinical chemotherapy. Chemotherapy. 2017;62:43–53.
  • Zhu X, Zhao H, Lin Z, et al. Functional studies of miR-130a on the inhibitory pathways of apoptosis in patients with chronic myeloid leukemia. Cancer Gene Ther. 2015;22:573–580.
  • Kurosu T, Wu N, Oshikawa G, et al. Enhancement of imatinib-induced apoptosis of BCR/ABL-expressing cells by nutlin-3 through synergistic activation of the mitochondrial apoptotic pathway. Apoptosis. 2010;15:608–620.
  • Peterson LF, Mitrikeska E, Giannola D, et al. p53 stabilization induces apoptosis in chronic myeloid leukemia blast crisis cells. Leukemia. 2011;25:761–769.
  • Kusio-Kobialka M, Wolanin K, Podszywalow-Bartnicka P, et al. Increased acetylation of lysine 317/320 of p53 caused by BCR-ABL protects from cytoplasmic translocation of p53 and mitochondria-dependent apoptosis in response to DNA damage. Apoptosis. 2012;17:950–963.
  • Shafagh M, Rahmani F, Delirezh N. CuO nanoparticles induce cytotoxicity and apoptosis in human K562 cancer cell line via mitochondrial pathway, through reactive oxygen species and P53. Iran J Basic Med Sci. 2015;18:993–1000.

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