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Research Article

Sorafenib regulates c-CBL gene-mediated chemoresistance in acute myeloid leukemia cells

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Article: 2204620 | Received 09 Jan 2023, Accepted 15 Apr 2023, Published online: 18 May 2023

References

  • O'Dwyer K, Freyer DR, Horan JT. Treatment strategies for adolescent and young adult patients with acute myeloid leukemia. Blood. 2018;132(4):362–368.
  • Grimwade D, Ivey A, Huntly BJ. Molecular landscape of acute myeloid leukemia in younger adults and its clinical relevance. Blood. 2016;127(1):29–41.
  • Gebru MT, Wang HG. Therapeutic targeting of FLT3 and associated drug resistance in acute myeloid leukemia. J Hematol Oncol. 2020;13(1):155.
  • Sasaki K, Kantarjian HM, Kadia T, et al. Sorafenib plus intensive chemotherapy improves survival in patients with newly diagnosed, FLT3-internal tandem duplication mutation-positive acute myeloid leukemia. Cancer. 2019;125(21):3755–-3766.
  • Daver N, Konopleva M. Sorafenib and novel multikinase inhibitors in AML. Lancet Oncol. 2015;16(16):1582–1583.
  • Pratz KW, Rudek MA, Smith BD, et al. A prospective study of peritransplant sorafenib for patients with FLT3-ITD acute myeloid leukemia undergoing allogeneic transplantation. Biol Blood Marrow Transplant. 2020;26(2):300–306.
  • De Freitas T, Marktel S, Piemontese S, et al. High rate of hematological responses to sorafenib in FLT3-ITD acute myeloid leukemia relapsed after allogeneic hematopoietic stem cell transplantation. Eur J Haematol. 2016;96(6):629–636.
  • Gatzka MV. Targeted tumor therapy remixed-an update on the use of small-molecule drugs in combination therapies. Cancers (Basel). 2018;10(6).
  • Uy GL, Mandrekar SJ, Laumann K, et al. A phase 2 study incorporating sorafenib into the chemotherapy for older adults with FLT3-mutated acute myeloid leukemia: CALGB 11001. Blood Adv. 2017;1(5):331–340.
  • Liu XS, Long H, Huang YX, et al. [Clinical efficacy of sorafenib combined with low dose cytarabine for treating patients with FLT3+ relapsed and refractory acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2016;24(2):394–398.
  • Taylor SJ, Thien CB, Dagger SA, et al. Loss of c-Cbl E3 ubiquitin ligase activity enhances the development of myeloid leukemia in FLT3-ITD mutant mice. Exp Hematol. 2015;43(3):191–206. e191.
  • Liyasova MS, Ma K, Lipkowitz S. Molecular pathways: cbl proteins in tumorigenesis and antitumor immunity-opportunities for cancer treatment. Clin Cancer Res. 2015;21(8):1789–1794.
  • Katzav S, Schmitz ML. Mutations of c-Cbl in myeloid malignancies. Oncotarget. 2015;6(13):10689–10696.
  • Sun J, Pedersen M, Bengtsson S, et al. Grb2 mediates negative regulation of stem cell factor receptor/c-Kit signaling by recruitment of Cbl. Exp Cell Res. 2007;313(18):3935–3942.
  • Ahmed SF, Buetow L, Gabrielsen M, et al. E3 ligase-inactivation rewires CBL interactome to elicit oncogenesis by hijacking RTK-CBL-CIN85 axis. Oncogene. 2021;40(12):2149–2164.
  • Liu J, Yang L, He A, et al. Stable and EGF-induced temporal interactome profiling of CBL and CBLB highlights their signaling complex diversity. J Proteome Res. 2021;20(7):3709–3719.
  • Lyle CL, Belghasem M. Chitalia VC. c-Cbl: an important regulator and a target in angiogenesis and tumorigenesis. Cells. 2019;8(5):498.
  • Mohapatra B, Ahmad G, Nadeau S, et al. Protein tyrosine kinase regulation by ubiquitination: critical roles of Cbl-family ubiquitin ligases. Biochim Biophys Acta. 2013;1833(1):122–139.
  • Sanada M, Suzuki T, Shih LY, et al. Gain-of-function of mutated C-CBL tumour suppressor in myeloid neoplasms. Nature. 2009;460(7257):904–908.
  • Kales SC, Ryan PE, Nau MM, et al. Cbl and human myeloid neoplasms: the Cbl oncogene comes of age. Cancer Res. 2010;70(12):4789–4794.
  • Ogawa S, Shih LY, Suzuki T, et al. Deregulated intracellular signaling by mutated c-CBL in myeloid neoplasms. Clin Cancer Res. 2010;16(15):3825–3831.
  • Marklin M, Tandler C, Kopp HG, et al. C-Cbl regulates c-MPL receptor trafficking and its internalization. J Cell Mol Med. 2020;24(21):12491–12503.
  • Chen S, Sun Q, Sun D, et al. C-CBL is required for inhibition of angiogenesis through modulating JAK2/STAT3 activity in ROP development. Biomed Pharmacother. 2020;132:110856.
  • Nadeau SA, An W, Mohapatra BC, et al. Structural determinants of the gain-of-function phenotype of human leukemia-associated mutant CBL oncogene. J Biol Chem. 2017;292(9):3666–3682.
  • Yawut N, Kaewpiboon C, Budluang P, et al. Overexpression of cancer upregulated gene 2 (CUG2) decreases Spry2 through c-Cbl, leading to activation of EGFR and beta-catenin signaling. Cancer Manag Res. 2020;12:10243–10250.
  • Lyle CL, Belghasem M. Chitalia VC. c-Cbl: an important regulator and a target in angiogenesis and tumorigenesis. Cells. 2019;8(5).
  • Galanis A, Levis M. Inhibition of c-Kit by tyrosine kinase inhibitors. Haematologica. 2015;100(3):e77–79.
  • Zeng S, Xu Z, Lipkowitz S, et al. Regulation of stem cell factor receptor signaling by CBL family proteins (Cbl-b/c-Cbl). Blood. 2005;105(1):226–232.
  • Dikic I, Giordano S. Negative receptor signalling. Curr Opin Cell Biol. 2003;15(2):128–135.
  • Jang HD, Hwang HZ, Kim HS, et al. C-Cbl negatively regulates TRAF6-mediated NF-kappaB activation by promoting K48-linked polyubiquitination of TRAF6. Cell Mol Biol Lett. 2019;24:29.
  • Crotchett BLM, Ceresa BP. Knockout of c-Cbl slows EGFR endocytic trafficking and enhances EGFR signaling despite incompletely blocking receptor ubiquitylation. Pharmacol Res Perspect. 2021;9(2):e00756.
  • Lee V, Griffin TD, Suzuki-Horiuchi Y, et al. Downregulation of Src-family tyrosine kinases by Srcasm and c-Cbl: a comparative analysis. J Carcinog. 2021;20:21.
  • Claudio AP, Joazeiro SSW, Huang H-k, et al. The tyrosine kinase negative regulator c-Cbl as a RING-Type, E2-dependent ubiquitin-protein ligase. Full. 1999;286:8.
  • Langdon WY, Klinken SP, Ruscetti SK. Morse HC v-cbl, an oncogene from a dual-recombinant urine retrovirus that induces early B-lineage lymphomas. Proc Natl Acad Sci USA. 1989;86(4):1168–1172.
  • Lindblad O, Cordero E, Puissant A, et al. Aberrant activation of the PI3K/mTOR pathway promotes resistance to sorafenib in AML. Oncogene. 2016;35(39):5119–5131.
  • Fouladi F, Jehn LB, Metzelder SK, et al. Sorafenib induces paradoxical phosphorylation of the extracellular signal-regulated kinase pathway in acute myeloid leukemia cells lacking FLT3-ITD mutation. Leuk Lymphoma. 2015;56(9):2690–2698.
  • Allen C, Hills RK, Lamb K, et al. The importance of relative mutant level for evaluating impact on outcome of KIT, FLT3 and CBL mutations in core-binding factor acute myeloid leukemia. Leukemia. 2013;27(9):1891–1901.
  • Rorsman C, Tsioumpekou M, Heldin CH, et al. The ubiquitin ligases c-Cbl and Cbl-b negatively regulate platelet-derived growth factor (PDGF) BB-induced chemotaxis by affecting PDGF receptor beta (PDGFRbeta) internalization and signaling. J Biol Chem. 2016;291(22):11608–11618.
  • Belizaire R, Koochaki SHJ, Udeshi ND, et al. CBL mutations drive PI3K/AKT signaling via increased interaction with LYN and PIK3R1. Blood. 2021;137(16):2209–2220.
  • Beretta GL, Cassinelli G, Pennati M, et al. Overcoming ABC transporter-mediated multidrug resistance: the dual role of tyrosine kinase inhibitors as multitargeting agents. Eur J Med Chem. 2017;142:271–289.
  • Eadie LN, Hughes TP, White DL. Interaction of the efflux transporters ABCB1 and ABCG2 with imatinib, nilotinib, and dasatinib. Clin Pharmacol Ther. 2014;95(3):294–306.
  • Dohse M, Scharenberg C, Shukla S, et al. Comparison of ATP-binding cassette transporter interactions with the tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib. Drug Metab Dispos. 2010;38(8):1371–1380.