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Impact of carboxymethyl dextran-asparaginase in NALM-6 cell apoptosis and autophagy | ||
| Iranian Journal of Veterinary Research | ||
| دوره 25، شماره 4 - شماره پیاپی 89، 2024، صفحه 344-352 اصل مقاله (455.46 K) | ||
| نوع مقاله: Full paper (Original article) | ||
| شناسه دیجیتال (DOI): 10.22099/ijvr.2024.49166.7208 | ||
| نویسندگان | ||
| M. Azizian1؛ G. H. Tamaddon2؛ M. Ashrafi* 3؛ M. Chahardahcherik1؛ F. Gharechahi4 | ||
| 1Ph.D. Student in Biochemistry, Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran | ||
| 2Department of Laboratory Sciences, Faculty of Paramedical Sciences, Shiraz University of Medical Sciences and Health Services, Shiraz, Iran | ||
| 3Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran | ||
| 4MSc Student in Hematology, Department of Laboratory Sciences, Faculty of Paramedical Sciences, Shiraz University of Medical Sciences and Health Services, Shiraz, Iran | ||
| چکیده | ||
| Background: Acute lymphoblastic leukemia (ALL) is a malignant disorder in both humans and animals. L-asparaginase (L-ASNase) has limitations as a chemotherapy agent due to adverse effects and low serum stability. In a previous study, L-ASNase was chemically modified with carboxymethyl dextran to enhance its properties. Aims: This study aimed to validate the potential of these modifications using the NALM-6 cell line. Methods: NALM-6 cells were cultured and treated with various concentrations, including 0 IU/ml as negative control, 0.5, 1, 1.5, and 2 IU/ml of modified L-ASNase and L-ASNase. The optimal concentration was determined at specific intervals, and viability and metabolic activity were assessed through Trypan blue and MTT tests. Flow cytometry, using Annexin V/PI staining, was employed to evaluate apoptosis. Real-time RT-PCR techniques were used to determine changes in the expression of the ATG2B and LC3-II genes (important genes in autophagy), with data analysis conducted using PRISM software. Results: The modified L-ASNase reduced the viability of NALM-6 cells and induced higher levels of apoptosis (P=0.001). Interestingly, the modified enzyme had a lesser impact on autophagy, which is important for avoiding treatment resistance. Conclusion: The modified L-ASNase showed enhanced effectiveness in reducing the viability of NALM-6 cells and induced higher levels of apoptosis. Interestingly, the modified enzyme had a lesser effect on autophagy, which is important as excessive autophagy can lead to treatment resistance. These findings suggest that the modified L-ASNase may have the potential to be a more effective chemotherapeutic agent for ALL treatments. | ||
| کلیدواژهها | ||
| Acute lymphoblastic leukemia؛ Apoptosis؛ Autophagy؛ L-asparaginase؛ NALM-6 cell line | ||
| مراجع | ||
|
Batool, T; Makky, EA; Jalal, M and Yusoff, MM (2016). A comprehensive review on L-asparaginase and its applications. Appl. Biochem. Biotechnol., 178: 900-923.
Belviso, S; Iuliano, R; Amato, R; Perrotti, N and Menniti, M (2017). The human asparaginase enzyme (ASPG) inhibits growth in leukemic cells. PloS One. 12: 0178174.
Bhat, P; Kriel, J; Shubha, B; Basappa, P; Shivananju, NS and Loos, B (2018). Modulating autophagy in cancer therapy: advancements and challenges for cancer cell death sensitization. Biochem. Pharmacol., 147: 170-182.
Cecconello, DK; Magalhães, MRD; Werlang, ICR; Lee, MLDM; Michalowski, MB and Daudt, LE (2020). Asparaginase: An old drug with new questions. Hematol. Transfus. Cell Ther., 42: 275-282.
Chahardahcherik, M; Ashrafi, M; Ghasemi, Y and Aminlari, M (2020). Effect of chemical modification with carboxymethyl dextran on kinetic and structural properties of L-asparaginase. Anal. Biochem., 591: 113537.
Chen, Q; Ye, L; Fan, J; Zhang, X; Wang, H; Liao, S; Song, P; Wang, Z; Wang, S and Li, Y (2017). Autophagy suppression potentiates the anti-glioblastoma effect of asparaginase in vitro and in vivo. Oncotarget. 8: 91052-91066.
Cuomo, F; Altucci, L and Cobellis, G (2019). Autophagy function and dysfunction: potential drugs as anti-cancer therapy. Cancers. 11: 1465.
Denton, D; Xu, T and Kumar, S (2015). Autophagy as a pro-death pathway. Immunol. Cell Biol., 93: 35-42.
Galluzzi, L; Baehrecke, EH; Ballabio, A; Boya, P; Bravo-San Pedro, JM; Cecconi, F; Choi, AM; Chu, CT; Codogno, P and Colombo, MI (2017). Molecular definitions of autophagy and related processes. EMBO J., 36: 1811-1836.
Gharehchahi, F; Zare, F; Dehbidi, GR; Yousefi, Z; Pourpirali, S and Tamaddon, G (2023). Autophagy and apoptosis cross-talk in response to epigallocatechin gallate in NALM-6 cell line. Jundishapur J. Nat. Pharm. Prod., 18: e138054.
Hlozkova, K; Pecinova, A; Alquezar-Artieda, N; Pajuelo-Reguera, D; Simcikova, M; Hovorkova, L; Rejlova, K; Zaliova, M; Mracek, T and Kolenova, A (2020). Metabolic profile of leukemia cells influences treatment efficacy of L-asparaginase. BMC Cancer. 20: 1-13.
Huang, X; Bai, HM; Chen, L; Li, B and Lu, YC (2010). Reduced expression of LC3B-II and beclin 1 in glioblastoma multiforme indicates a down-regulated autophagic capacity that relates to the progression of astrocytic tumors. J. Clin. Neurosci., 17: 1515-1519.
Iacobucci, I and Mullighan, CG (2017). Genetic basis of acute lymphoblastic leukemia. J. Clin. Oncol., 35: 975-983.
Jia, B; Xue, Y; Yan, X; Li, J; Wu, Y; Guo, R; Zhang, J; Zhang, L; Li, Y and Liu, Y (2018). Autophagy inhibitor chloroquine induces apoptosis of cholangiocarcinoma cells via endoplasmic reticulum stress. Oncol. Lett., 16: 3509-3516.
Lee, JJ; Liao, AT and Wang, SL (2021). L-Asparaginase, doxorubicin, vincristine, and prednisolone (LHOP) chemotherapy as a first-line treatment for dogs with multicentric lymphoma. Animals. 11: 2199.
Lin, XT; Zheng, XB; Fan, DJ; Yao, QQ; Hu, JC; Lian, L; Wu, XJ; Lan, P and He, XS (2018). MicroRNA-143 targets ATG2B to inhibit autophagy and increase inflammatory responses in Crohn’s disease. Inflamm. Bowel Dis., 24: 781-791.
Livak, KJ and Schmittgen, TD (2001). Analysis of relative gene expression data using real-time quantitative PCR and the 2-ΔΔCT method. Methods. 25: 402-408.
Mauthe, M; Orhon, I; Rocchi, C; Zhou, X; Luhr, M; Hijlkema, KJ; Coppes, RP; Engedal, N; Mari, M and Reggiori, F (2018). Chloroquine inhibits autophagic flux by decreasing autophagosome-lysosome fusion. Autophagy. 14: 1435-1455.
Métayer, LE; Brown, RD; Carlebur, S; Burke, GA and Brown, GC (2019). Mechanisms of cell death induced by arginase and asparaginase in precursor B-cell lymphoblasts. Apoptosis. 24: 145-156.
Mohan Kumar, N; Kishore, V and Manonmani, H (2014). Chemical modification of L-asparaginase from Cladosporium sp. for improved activity and thermal stability. Prep. Biochem. Biotechnol., 44: 433-450.
Noda, NN and Inagaki, F (2015). Mechanisms of autophagy. Annu. Rev. Biophys., 44: 101-122.
Parmentier, JH; Maggi, M; Tarasco, E; Scotti, C; Avramis, VI and Mittelman, SD (2015). Glutaminase activity determines cytotoxicity of L-asparaginases on most leukemia cell lines. Leuk. Res., 39: 757-762.
Parzych, KR and Klionsky, DJ (2014). An overview of autophagy: morphology, mechanism, and regulation. ARS., 20: 460-473.
Piatkowska-Jakubas, B; Krawczyk-Kuliś, M; Giebel, S; Adamczyk-Cioch, M; Czyz, A; Lech, ME; Paluszewska, M; Pałynyczko, G; Piszcz, J and Hołowiecki, J (2008). Use of L-asparaginase in acute lymphoblastic leukemia: recommendations of the polish adult leukemia group. Pol. Arch. Med. Wewn., 118: 664-669.
Ravikumar, B; Sarkar, S; Davies, JE; Futter, M; Garcia-Arencibia, M; Green-Thompson, ZW; Jimenez-Sanchez, M; Korolchuk, VI; Lichtenberg, M and Luo, S (2010). Regulation of mammalian autophagy in physiology and pathophysiology. Physiol. Rev., 90: 1383-1435.
Rizzari, C; Citterio, M; Zucchetti, M; Conter, V; Chiesa, R; Colombini, A; Malguzzi, S; Silvestri, D and D'Incalci, M (2006). A pharmacological study on pegylated asparaginase used in front-line treatment of children with acute lymphoblastic leukemia. Haematologica. 91: 24-31.
Sever, ON and Demir, OG (2017). Autophagy: Cell death or survive mechanism. J. Oncol. Sci., 3: 37-44.
Shafique, S and Tehsin, S (2018). Acute lymphoblastic leukemia detection and classification of its subtypes using pretrained deep convolutional neural networks. Technol. Cancer Res. Treat., 17: 1533033818802789.
Soares, AL; Guimaraes, GM; Polakiewicz, B; De Moraes Pitombo, RN and Abrahão-Neto, J (2002). Effects of polyethylene glycol attachment on physicochemical and biological stability of E. coli L-asparaginase. Int. J. Pharm., 237: 163-170.
Song, P; Ye, L; Fan, J; Li, Y; Zeng, X; Wang, Z; Wang, S; Zhang, G; Yang, P and Cao, Z (2015). Asparaginase induces apoptosis and cytoprotective autophagy in chronic myeloid leukemia cells. Oncotarget. 6: 3861-3873.
Suter, SE; Small, GW; Seiser, EL; Thomas, R; Breen, M and Richards, KL (2011). FLT3 mutations in canine acute lymphocytic leukemia. BMC Cancer. 11: 1-8.
Tabandeh, MR and Aminlari, M (2009). Synthesis, physicochemical and immunological properties of oxidized inulin–l-asparaginase bioconjugate. J. Biotechnol., 141: 189-195.
Tandel, P; Ranjbaran, R; Ebrahimi, E; Rezvani, A; Ramzi, M and Tamaddon, G (2022). Decreased expression of autophagy-related genes in the complete remission phase of acute myeloid leukemia. Mol. Genet. Genomic Med., 10: 1872-1881.
Tufekci, E; Ekinci, G and Keleş, I (2022). Leukemia in dogs. Bozok Vet. Sci., 3: 20-27.
Ullmannova, V and Haskovec, C (2003). The use of housekeeping genes (HKG) as an internal control for the detection of gene expression by quantitative real-time RT-PCR. Folia Biol., 49: 211-216.
Velikkakath, AKG; Nishimura, T; Oita, E; Ishihara, N and Mizushima, N (2012). Mammalian Atg2 proteins are essential for autophagosome formation and important for regulation of size and distribution of lipid droplets. Mol. Biol. Cell., 23: 896-909.
Wang, N; Ji, W; Wang, L; Wu, W; Zhang, W; Wu, Q; Du, W; Bai, H; Peng, B and Ma, B (2022). Overview of the structure, side effects, and activity assays of l-asparaginase as a therapy drug of acute lymphoblastic leukemia. RSC Med. Chem., 13: 117-128.
Wang, R and Wang, G (2019). Protein modification and autophagy activation. Adv. Exp. Med. Biol., 1206: 237-259. doi: 10.1007/978-981-15-0602-4_12.
Wirawan, E; Berghe, TV; Lippens, S; Agostinis, P and Vandenabeele, P (2012). Autophagy: for better or for worse. Cell Res., 22: 43-61.
Yang, Y and Klionsky, DJ (2020). Autophagy and disease: Unanswered questions. Cell Death Differ., 27: 858-871.
Yorimitsu, T and Klionsky, DJ (2005). Autophagy: molecular machinery for self-eating. Cell Death Differ., 12: 1542-1552.
Yu, L; Chen, Y and Tooze, SA (2018). Autophagy pathway: cellular and molecular mechanisms. Autophagy. 14: 207-215.
Zaffagnini, G and Martens, S (2016). Mechanisms of selective autophagy. JMB., 428: 1714-1724. Zhang, JF; Shi, LY and Wei, DZ (2004). Chemical modification of L-asparaginase from Escherichia coli with a modified polyethyleneglycol under substrate protection conditions. Biotechnol. Lett., 26: 753-756.
Zhou, R; Liang, T; Li, T; Huang, J and Chen, C (2023). Possible mechanism of metabolic and drug resistance with L-asparaginase therapy in childhood leukaemia. Front. Oncol., 13: 1070069. | ||
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