(1) Tu WB, Helander S, Pilstål R, Hickman KA,Lourenco C, Jurisica I, Raught B, Wallner B,Sunnerhagen M and Penn LZ. Myc and its interactorstake shape. Biochim. Biophys. Acta (2015) 1849:469-83.
(2) Kress TR, Sabò A and Amati B. MYC: connectingselective transcriptional control to global RNAproduction. Nat. Rev. Cancer (2015) 15: 593.
(3) Meyer N and Penn LZ. Reflecting on 25 years withMYC. Nat. Rev. Cancer (2008) 8: 976.
(4) Akyurek N, Uner A, Benekli M and Barista I.Prognostic significance of MYC, BCL2, and BCL6rearrangements in patients with diffuse large B‐cell lymphoma treated with cyclophosphamide,doxorubicin, vincristine, and prednisone plusrituximab. Cancer (2012) 118: 4173-83.
(5) Nagy B, Lundán T, Larramendy ML, Aalto Y, ZhuY, Niini T, Edgren H, Ferrer A, Vilpo J and ElonenE. Abnormal expression of apoptosis‐related genesin haematological malignancies: overexpression of MYC is poor prognostic sign in mantle cellFigure 8. Schematic representation proposed for the plausible mechanisms of action of 10058-F4 in APL-derivedNB4 cells.Through inhibition of c-Myc, 10058-F4 augmented the intracellular level of ROS and induced caspase-3-dependent apoptotic cell death in NB4 cells through suppression of the NF-κB signaling pathway. This favorableanti-leukemic activity could be attenuated through activation of the PI3K signaling pathway. Suppression of thePI3K axis using CAL-101 eliminated the compensatory effect of this pathway on 10058-F4-induced cytotoxic effect and promoted a more significant apoptotic cell death in NB4 cells. Figure 8. Schematic representation proposed for the plausible mechanisms of action of 10058-F4 in APL-derived NB4 cells. Through inhibition of c-Myc, 10058-F4 augmented the intracellular level of ROS and induced caspase-3-dependent apoptotic cell death in NB4 cells through suppression of the NF-κB signaling pathway. This favorable anti-leukemic activity could be attenuated through activation of the PI3K signaling pathway. Suppression of the PI3K axis using CAL-101 eliminated the compensatory effect of this pathway on 10058-F4-induced cytotoxic effect and promoted a more significant apoptotic cell death in NB4 cells. 164 Sayyadi M et al. / IJPR (2020), 19 (1): 153-165 lymphoma. Br. J. Haematol. (2003) 120: 434-41.
(6) Luo H, Li Q, O’Neal J, Kreisel F, Le Beau MM and Tomasson MH. c-Myc rapidly induces acute myeloid leukemia in mice without evidence of lymphomaassociated antiapoptotic mutations. Blood (2005) 106: 2452-61.
(7) Alitalo K, Winqvist R, Keski-Oja J, Ilvonen M, Saksela K, Alitalo R, Laiho M, Knuutila S and De La Chapelle A. Acute myelogenous leukaemia with c-myc amplification and double minute chromosomes. Lancet (1985) 326: 1035-9.
(8) Schick M, Habringer S, Nilsson JA and Keller U. Pathogenesis and therapeutic targeting of aberrant MYC expression in haematological cancers. Br. J. Haematol. (2017) 179: 724-38.
(9) Carabet LA, Lallous N, Leblanc E, Ban F, Morin H, Lawn S, Ghaidi F, Lee J, Mills IG and Gleave ME. Computer-aided drug discovery of Myc-Max inhibitors as potential therapeutics for prostate cancer. Eur. J. Med. Chem. (2018) 160: 108-19.
(10) Wang J, Ma X, Jones HM, Chan LLY, Song F, Zhang W, Bae-Jump VL and Zhou C. Evaluation of the antitumor effects of c-Myc-Max heterodimerization inhibitor 100258-F4 in ovarian cancer cells. J. Transl. Med. (2014) 12: 226.
(11) Lin CP, Liu JD, Chow JM, Liu CR and Liu HE. Small-molecule c-Myc inhibitor, 10058-F4, inhibits proliferation, downregulates human telomerase reverse transcriptase and enhances chemosensitivity in human hepatocellular carcinoma cells. Anticancer Drugs (2007) 18: 161- 70.
(12) Kleszcz R, Paluszczak J, Krajka-Kuzniak V and Baer-Dubowska W. The inhibition of c-MYC transcription factor modulates the expression of glycolytic and glutaminolytic enzymes in FaDu hypopharyngeal carcinoma cells. Adv. Clin. Exp. Med. (2018) 27: 735-42.
(13) Bashash D, Sayyadi M, Safaroghli-Azar A, Sheikh-Zeineddini N, Riyahi N and Momeny M. Small molecule inhibitor of c-Myc 10058- F4 inhibits proliferation and induces apoptosis in acute leukemia cells, irrespective of PTEN status. Int. J. Biochem. Cell Biol. (2019) 108: 7-16.
(14) Sheikh‐Zeineddini N, Bashash D, Safaroghli‐Azar A, Riyahi N, Shabestari RM, Janzamin E and Safa M. Suppression of c‐Myc using 10058‐F4 exerts caspase‐3‐dependent apoptosis and intensifies the antileukemic effect of vincristine in pre‐B acute lymphoblastic leukemia cells. J. Cell. Biochem. (2019) 120: 14004-16.
(15) Riyahi N, Safaroghli-Azar A, Sheikh-Zeineddini N, Sayyadi M and Bashash D. Synergistic effects of PI3K and c-Myc co-targeting in acute leukemia: shedding new light on resistance to selective PI3K-δ inhibitor CAL-101. Cancer Invest. (2019) 37: 311-24.
(16) Tan Y, Sementino E, Chernoff J and Testa JR. Targeting MYC sensitizes malignant mesothelioma cells to PAK blockage-induced cytotoxicity. Am. J. Cancer Res. (2017) 7: 1724-37.
(17) Zhao Q, Assimopoulou AN, Klauck SM, Damianakos H, Chinou I, Kretschmer N, Rios JL, Papageorgiou VP, Bauer R and Efferth T. Inhibition of c-MYC with involvement of ERK/JNK/MAPK and AKT pathways as a novel mechanism for shikonin and its derivatives in killing leukemia cells. Oncotarget (2015) 6: 38934-51.
(18) Sheikh‐Zeineddini N, Safaroghli-Azar A, Salari Sand Bashash D. C-Myc inhibition sensitizes pre-B ALL cells to the anti-tumor effect of vincristine
by altering apoptosis and autophagy: Proposing a probable mechanism of action for 10058-F4. Eur. J. Pharmacol. (2019) 172821.
(19) Prochownik EV. c-Myc as a therapeutic target in cancer. Expert Rev. Anticancer Ther. (2004) 4: 289- 302.
(20) Ho JS, Ma W, Mao DY and Benchimol S. p53- Dependent transcriptional repression of c-myc isrequired for G1 cell cycle arrest. Mol. Cell Biol.
(2005) 25: 7423-31.
(21) Khan S, Lopez-Dee Z, Kumar R and Ling J.Activation of NFkB is a novel mechanism of prosurvival activity of glucocorticoids in breast cancercells. Cancer Lett. (2013) 337: 90-5.
(22) Bubici C, Papa S, Pham C, Zazzeroni F andFranzoso G. The NF-kB-mediated control of ROSand JNK signaling. Histol. Histopathol. (2006) 21:69-80.
(23) Havens CG, Ho A, Yoshioka N and Dowdy SF.Regulation of late G1/S phase transition andAPCCdh1 by reactive oxygen species. Mol. CellBiol. (2006) 26: 4701-11.
(24) Codogno P and Meijer A. Autophagy and signaling:their role in cell survival and cell death. Cell DeathDiffer. (2005) 12 (Suppl 2): 1509-18.
(25) Harashima N, Inao T, Imamura R, Okano S, Suda Tand Harada M. Roles of the PI3K/Akt pathway andautophagy in TLR3 signaling-induced apoptosisand growth arrest of human prostate cancer cells.Cancer Immunol. Immunother. (2012) 61: 667-76.
(26) Balakumaran BS, Porrello A, Hsu DS, Glover W,Foye A, Leung JY, Sullivan BA, Hahn WC, LodaM and Febbo PG. MYC activity mitigates responseto rapamycin in prostate cancer through eukaryoticinitiation factor 4E–binding protein 1–mediatedinhibition of autophagy. Cancer Res. (2009) 69:7803-10.165NF-κB-dependent Mechanism of -Myc inhibitor 10058-F4 in APL cells
(27) Suzuki-Karasaki Y, Suzuki-Karasaki M, UchidaM and Ochiai T. Depolarization controls TRAILsensitization and tumor-selective killing of cancercells: crosstalk with ROS. Front. Oncol. (2014) 4:128.
(28) Bashash D, Safaroghli-Azar A, Delshad M, BayatiS, Nooshinfar E and Ghaffari SH. Inhibitor ofpan class-I PI3K induces differentially apoptoticpathways in acute leukemia cells: Shedding newlight on NVP-BKM120 mechanism of action. Int.J. Biochem. Cell Biol. (2016) 79: 308-17.
(29) Bashash D, Safaroghli-Azar A, Dadashi M, Safa M,Momeny M and Ghaffari SH. Anti-tumor activityof PI3K-δ inhibitor in hematologic malignant cells:shedding new light on resistance to Idelalisib. Int.J. Biochem. Cell Biol. (2017) 85: 149-58.
(30) Wang J and Yi J. Cancer cell killing via ROS: toincrease or decrease, that is the question. CancerBoil. Ther. (2008) 7: 1875-84.
(31) Sui X, Chen R, Wang Z, Huang Z, Kong N, Zhang M, Han W, Lou F, Yang J and Zhang Q. Autophagy and chemotherapy resistance: a promising therapeutic target for cancer treatment. Cell Death Dis. (2013) 4: e838