Synergy between parthenolide and arsenic trioxide in adult T-cell leukemia/lymphoma cells in vitro | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 8، دوره 23، شماره 5، مرداد 2020، صفحه 616-622 اصل مقاله (742.38 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2020.40650.9610 | ||
| نویسندگان | ||
| Hamideh Kouhpaykar1؛ Mohammad Hadi Sadeghian1؛ Houshang Rafatpanah2؛ Mohadeseh Kazemi2؛ Mehrdad Iranshahi3؛ Zahra Delbari2؛ Faezeh Khodadadi1؛ Hossein Ayatolahi1؛ Fatemeh B. Rassouli* 4 | ||
| 1Cancer Molecular Pathology Research Center, Department of Hematology and Blood Bank, Faculty of Medicine, Mashhad University of Medical Sciences, Iran | ||
| 2Inflammation and Inflammatory Diseases Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran | ||
| 3Department of Pharmacognosy and Biotechnology, Biotechnology Research Center, Faculty of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran | ||
| 4Novel Diagnostics and Therapeutics Research Group, Institute of Biotechnology, Ferdowsi University of Mashhad, Mashhad, Iran | ||
| چکیده | ||
| Objective(s): Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoid malignancy with low survival rate and distinct geographical distribution. In search for novel chemotherapeutics against ATLL, we investigated the combinatorial effects of parthenolide, a sesquiterpene lactone with valuable pharmaceutical activities, and arsenic trioxide (ATO) in vitro. Materials and Methods: MT2 cells, an ATLL cell line, were treated with increasing concentrations of parthenolide (1.25, 2.5, and 5 μg/ml) and ATO (2, 4, 8, and 16 µM) to determine their IC50. Then, cells were treated with a combination of sub-IC50 concentrations of parthenolide (1 μg/ml) and ATO (2 µM) for 72 hr. Cell viability and cell cycle changes were assessed by Alamar blue and PI staining, respectively. To understand the mechanisms responsible for observed effects, expression of CD44, NF-κB (REL-A), BMI-1, and C-MYC were investigated by real-time PCR. Results: Assessment of cell viability indicated that parthenolide significantly increased the toxicity of ATO, as confirmed by accumulation of MT2 cells in the sub G1 phase of the cell cycle. Moreover, molecular analysis revealed significant down-regulation of CD44, NF-κB (REL-A), BMI-1, and C-MYC upon combinatorial administration of parthenolide and ATO in comparison with relevant controls. Conclusion: Taken together, present results showed that parthenolide significantly enhanced the toxicity of ATO in MT2 cells. Therefore, the future possible clinical impact of our study could be combinatorial use of parthenolide and ATO as a novel and more effective approach for ATLL. | ||
| کلیدواژهها | ||
| Adult T-cell Leukemia/Lymphoma؛ Arsenic Trioxide؛ In vitro؛ Parthenolide؛ PCR | ||
| مراجع | ||
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1. Martin JL, Maldonado JO, Mueller JD, Zhang W, Mansky LM. Molecular studies of HTLV-1 replication: An update. Viruses. 2016; 8:31-37. 2. Utsunomiya A, Choi I, Chihara D, Seto M. Recent advances in the treatment of adult T‐cell leukemia‐lymphomas. Cancer Sci. 2015; 106:344-351. 3. Yared JA, Kimball AS. Optimizing management of patients with adult T cell leukemia-lymphoma. Cancers (Basel). 2015; 7:2318-2329. 4. Bittencourt AL, Vieira MdG, Brites CR, Farre L, Barbosa HS. Adult T-cell leukemia/lymphoma in Bahia, Brazil: analysis of prognostic factors in a group of 70 patients. Am J Clin Pathol. 2007; 128:875-882. 5. Ishitsuka K, Tamura K. Human T-cell leukaemia virus type I and adult T-cell leukaemia-lymphoma. Lancet Oncol. 2014; 15:e517-e526. 6. Kchour G, Tarhini M, Kooshyar M-M, El Hajj H, Wattel E, Mahmoudi M, et al. Phase 2 study of the efficacy and safety of the combination of arsenic trioxide, interferon alpha, and zidovudine in newly diagnosed chronic adult T-cell leukemia/lymphoma (ATL). Blood. 2009; 113:6528-6532. 7. Bazarbachi A, Suarez F, Fields P, Hermine O. How I treat adult T-cell leukemia/lymphoma. Blood. 2011; 118:1736-1745. 8. Parada-Turska J, Paduch R, Majdan M, Kandefer-Szerszeñ M, Rzeski W. Antiproliferative activity of parthenolide against three human cancer cell lines and human umbilical vein endothelial cells. Pharmacol Rep. 2007; 59:233. 9. Dey S, Sarkar M, Giri B. Anti-inflammatory and anti-tumor activities of parthenolide: an update. J Chem Biol Ther. 2016; 2:1-6. 10. Taleghani A, Nasseri MA, Iranshahi M. Synthesis of dual-action parthenolide prodrugs as potent anticancer agents. Bioorg Chem. 2017; 71:128-134. 11. Hayashi S, Koshiba K, Hatashita M, Sato T, Jujo Y, Suzuki R, et al. Thermosensitization and induction of apoptosis or cell-cycle arrest via the MAPK cascade by parthenolide, an NF-κB inhibitor, in human prostate cancer androgen-independent cell lines. Int J Mol Med. 2011; 28:1033-1042. 12. Liu JW, Cai MX, Xin Y, Wu QS, Ma J, Yang P, et al. Parthenolide induces proliferation inhibition and apoptosis of pancreatic cancer cells in vitro. J Exp Clin Cancer Res. 2010; 29:108. 13. Zhang S, Ong C-N, Shen H-M. Critical roles of intracellular thiols and calcium in parthenolide-induced apoptosis in human colorectal cancer cells. Cancer Lett. 2004; 208:143-153. 14. Suvannasankha A, Crean CD, Shanmugam R, Farag SS, Abonour R, Boswell HS, et al. Antimyeloma effects of a sesquiterpene lactone parthenolide. Clin Cancer Res. 2008; 14:1814-1822. 15. Carlisi D, Lauricella M, D’Anneo A, Buttitta G, Emanuele S, Di Fiore R, et al. The synergistic effect of SAHA and parthenolide in MDA‐MB231 breast cancer cells. J Cell Physiol. 2015; 230:1276-1289. 16. Kim S-L, Kim SH, Trang KTT, Kim IH, Lee S-O, Lee ST, et al. Synergistic antitumor effect of 5-fluorouracil in combination with parthenolide in human colorectal cancer. Cancer Lett. 2013; 335:479-486. 17. Chou T, Martin N. CompuSyn software for drug combinations and for general dose-effect analysis, and user’s guide. Paramus: ComboSyn Inc 2007. 18. Kato S, Nishimura J, Muta K, Yufu Y, Nawata H, Ideguchi H. Overexpression of P-glycoprotein in adult T-cell leukaemia. Lancet. 1990; 336:573. 19. Sohma I, Fujiwara Y, Sugita Y, Yoshioka A, Shirakawa M, Moon J-H, et al. Parthenolide, an NF-κB inhibitor, suppresses tumor growth and enhances response to chemotherapy in gastric cancer. Cancer Genom Proteom. 2011; 8:39-47. 20. Wozniak M, Szulawska-Mroczek A, Hartman ML, Nejc D, Czyz M. Parthenolide complements the cell death-inducing activity of doxorubicin in melanoma cells. Anticancer Res. 2013; 33:3205-3212. 21. Zhang D, Qiu L, Jin X, Guo Z, Guo C. Nuclear factor-κB inhibition by parthenolide potentiates the efficacy of taxol in non–small cell lung cancer in vitro and in vivo. Mol Cancer Res. 2009; 7:1139-1149. 22. Liu D, Liu Y, Liu M, Ran L, Li Y. Reversing resistance of multidrug-resistant hepatic carcinoma cells with parthenolide. Future Oncol. 2013; 9:595-604. 23. Trang KTT, Kim S-L, Park S-B, Seo S-Y, Choi C-H, Park J-K, et al. Parthenolide sensitizes human colorectal cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through mitochondrial and caspase dependent pathway. Intestinal Res. 2014; 12:34-41. 24. Park WH, Seol JG, Kim ES, Hyun JM, Jung CW, Lee CC, et al. Arsenic trioxide-mediated growth inhibition in MC/CAR myeloma cells via cell cycle arrest in association with induction of cyclin-dependent kinase inhibitor, p21, and apoptosis. Cancer Res. 2000; 60:3065-3071. 25. Ralstin MC, Gage EA, Yip-Schneider MT, Klein PJ, Wiebke EA, Schmidt CM. Parthenolide cooperates with NS398 to inhibit growth of human hepatocellular carcinoma cells through effects on apoptosis and G0-G1 cell cycle arrest. Mol Cancer Res. 2006; 4:387-399. 26. Hoofd C, Wang X, Lam S, Jenkins C, Wood B, Giambra V, et al. CD44 promotes chemoresistance in T-ALL by increased drug efflux. Exp Hematol. 2016; 44:166-171. 27. Koopman G, Heider K, Horst E, Adolf G, Van Den Berg F, Ponta H, et al. Activated human lymphocytes and aggressive non-Hodgkin’s lymphomas express a homologue of the rat metastasis-associated variant of CD44. J Exp Med. 1993; 177:897-904. 28. Ghaffari S, Dougherty G, Eaves A, Eaves C. Altered patterns of CD44 epitope expression in human chronic and acute myeloid leukemia. Leukemia. 1996; 10:1773-1781. 29. Ghaffari S, Dougherty G, Lansdorp P, Eaves A, Eaves C. Differentiation-associated changes in CD44 isoform expression during normal hematopoiesis and their alteration in chronic myeloid leukemia. Blood. 1995; 86:2976-2985. 30. Chagan-Yasutan H, Tsukasaki K, Takahashi Y, Oguma S, Harigae H, Ishii N, et al. Involvement of osteopontin and its signaling molecule CD44 in clinicopathological features of adult T cell leukemia. Leukemia Res. 2011; 35:1484-1490. 31. Shih VF-S, Tsui R, Caldwell A, Hoffmann A. A single NFκB system for both canonical and non-canonical signaling. Cell Res. 2011; 21:86-102. 32. Rauch DA, Ratner L. Targeting HTLV-1 activation of NFκB in mouse models and ATLL patients. Viruses. 2011; 3:886-900. 33. Kim SL, Liu YC, Seo SY, Kim SH, Kim IH, Lee SO, et al. Parthenolide induces apoptosis in colitis-associated colon cancer, inhibiting NF-κB signaling. Oncol Let. 2015; 9:2135-2142. 34. Kong FC, Zhang JQ, Zeng C, Chen WL, Ren WX, Yan GX, et al. Inhibitory effects of parthenolide on the activity of NF-κB in multiple myeloma via targeting TRAF6. J Huazhong Uni Sci Technol. 2015; 35:343-349. 35. Kim S-L, Kim SH, Park YR, Liu Y-C, Kim E-M, Jeong H-J, et al. Combined parthenolide and balsalazide have enhanced antitumor efficacy through blockade of NF-κB activation. Mol Cancer Res. 2017; 15:141-151. 36. Yip-Schneider MT, Nakshatri H, Sweeney CJ, Marshall MS, Wiebke EA, Schmidt CM. Parthenolide and sulindac cooperate to mediate growth suppression and inhibit the nuclear factor-κB pathway in pancreatic carcinoma cells. Mol Cancer Ther. 2005; 4:587-594. 37. Dolcet X, Llobet D, Pallares J, Matias-Guiu X. NF-kB in development and progression of human cancer. Virchows Arch. 2005; 446:475-482. 38. Jiang L, Li J, Song L. Bmi-1, stem cells and cancer. Acta Biochim Biophys Sin. 2009; 41:527-534. 39. Bhattacharya R, Mustafi SB, Street M, Dey A, Dwivedi SKD. Bmi-1: At the crossroads of physiological and pathological biology. Genes Dis. 2015; 2:225-239. 40. Wang MC, Li CL, Cui J, Jiao M, Wu T, Jing L, et al. BMI‑1, a promising therapeutic target for human cancer. Oncol Lett. 2015; 10:583-588. 41. Molofsky AV, He S, Bydon M, Morrison SJ, Pardal R. Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways. Genes Dev. 2005; 19:1432-1437. 42. Bhattacharyya J, Mihara K, Ohtsubo M, Yasunaga Si, Takei Y, Yanagihara K, et al. Overexpression of BMI‐1 correlates with drug resistance in B‐cell lymphoma cells through the stabilization of survivin expression. Cancer Sci. 2012; 103:34-41. 43. Pelengaris S, Khan M, Evan G. c-MYC: more than just a matter of life and death. Nat Rev Cancer. 2002; 2:764-776. 44. Mihashi Y, Mizoguchi M, Takamatsu Y, Ishitsuka K, Iwasaki H, Koga M, et al. C-MYC and its main ubiquitin ligase, FBXW7, influence cell proliferation and prognosis in adult T-cell leukemia/lymphoma. Am J Surg Pathol. 2017; 41:1139-1149. 45. Li XY, Li Y, Zhang L, Liu X, Feng L, Wang X. The antitumor effects of arsenic trioxide in mantle cell lymphoma via targeting Wnt/β‑catenin pathway and DNA methyltransferase-1. Oncol Rep. 2017; 38:3114-3120. 46. HE Xl, HU Cl, MA Bl. The effection of arsenic trioxide in human lung adenocarcinoma A549 cell line proliferation and c-Myc gene expression. J Yanan Uni. 2013; 2:4-7. | ||
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