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:: Volume 24, Issue 6 (Bimonthly 2020) ::
Feyz Med Sci J 2020, 24(6): 601-609 Back to browse issues page
Effect of valproic acid on extrinsic (DR4, DR5, FAS, FAS-L, TRAIL) and intrinsic (BAX, BAK and APAF1, Bcl-2, and Bcl-xL) apoptotic pathways, cell viability and apoptosis in hepatocellular carcinoma PLC/PRF5 cell line
Masumeh Sanaei , Fraidoon Kavoosi *
Research Center for Non-Communicable Diseases, Jahrom University of Medical Sciences, Jahrom, I.R. Iran. , kavoosifraidoon@gmail.com
Abstract:   (1801 Views)
Background: Histone acetylation and deacetylation play an important role in transcription and gene expression. The acetylation status of histones and non-histone proteins is determined by histone acetyl-transferases (HATs) and histone deacetylases (HDACs). Histone deacetylase inhibitors (HDACIs) induce various molecular and extracellular effects, leading to potent anti-cancer activities. The current study was designed to investigate the effect of valproic acid) VPA( on extrinsic and intrinsic apoptotic pathways, cell viability, and apoptosis in hepatocellular carcinoma PLC/PRF5 cell line.
Materials and Methods: The hepatocellular carcinoma PLC/PRF5 was cultured. When cells approximately became 80% confluent, 3×105 cells were seeded into 96 and 24‑well plates. After 24 h, the medium was replaced with the medium contains VPA (except control groups which were treated with DMSO). After 24, 48, and 72 h, to determine cell viability, cell apoptosis and gene expression, MTT assay, flow cytometry and Real-time quantitative RT-PCR (qRT-PCR) were done respectively.
Results: VPA inhibited cell viability, induced apoptosis, decreased Bcl-2, and Bcl-xL and increased DR4, DR5, FAS, FAS-L, TRAIL, BAX, BAK and APAF1 significantly.
Conclusion: It seems that VPA can play its role through intrinsic and extrinsic apoptotic pathways in hepatocellular carcinoma PLC/PRF5 cell line.
Keywords: Valproic acid, Apoptotic pathway, Hepatocellular carcinoma, PLC/PRF5 CELL line
Full-Text [PDF 1560 kb]   (1326 Downloads)    
Type of Study: Research | Subject: medicine, paraclinic
Received: 2020/05/18 | Revised: 2021/02/8 | Accepted: 2020/10/13 | Published: 2021/02/8
References
1. Xu W, Parmigiani R, Marks P. Histone deacetylase inhibitors: molecular mechanisms of action. Oncogene 2007; 26(37): 5541-52.
2. Matthews GM, Newbold A, Johnstone RW. Intrinsic and extrinsic apoptotic pathway signaling as determinants of histone deacetylase inhibitor antitumor activity. Advances in cancer research. Elsevier 2012; 5: 165-97.
3. Eckschlager T, Plch J, Stiborova M, Hrabeta J. Histone deacetylase inhibitors as anticancer drugs. Int J Mol Sci 2017; 18(7): 1414.
4. Saharan R, Singh R, Nagar N, Verma S, Sharma V, Yadav S. HDAC inhibitors: a new armour in anti-cancer therapeutics. Pharmacophore 2011; 2: 104-13.
5. Facchetti F, Previdi S, Ballarini M, Minucci S, Perego P, La Porta C. Modulation of pro-and anti-apoptotic factors in human melanoma cells exposed to histone deacetylase inhibitors. Apoptosis 2004; 9(5): 573-82.
6. Meng J, Zhang HH, Zhou CX, Li C, Zhang F, Mei QB. The histone deacetylase inhibitor trichostatin A induces cell cycle arrest and apoptosis in colorectal cancer cells via p53-dependent and-independent pathways. Oncol Rep 2012; 28(1): 384-8.
7. Ryu JK, Lee WJ, Lee KH, Hwang JH, Kim YT, Yoon YB, et al. SK-7041, a new histone deacetylase inhibitor, induces G2-M cell cycle arrest and apoptosis in pancreatic cancer cell lines. Cancer Lett 2006; 237(1): 143-54.
8. Lee SH, Shin MS, Lee HS, Bae JH, Lee HK, Kim HS, et al. Expression of Fas and Fas-related molecules in human hepatocellular carcinoma. Hum Pathol 2001; 32(3): 250-6.
9. Sanaei M, Kavoosi F, Salehi H. Genistein and trichostatin a induction of estrogen receptor alpha gene expression, apoptosis and cell growth inhibition in hepatocellular carcinoma HepG 2 cells. Asian Pacific journal of cancer prevention: APJCP 2017; 18(12): 3445.
10. Sanaei M, Kavoosi F, Roustazadeh A, Golestan F. Effect of genistein in comparison with trichostatin a on reactivation of DNMTs genes in hepatocellular carcinoma. J Clin Transl Hepatol 2018; 6(2): 141–6.
11. Kavoosi F, Sanaei M. Comparative analysis of the effects of valproic acid and tamoxifen on proliferation, and apoptosis of human hepatocellular carcinoma WCH 17 celllin. Iran J Ped Hematol Oncol 2018; 8(1): 12-20.
12. Sanaei M, Kavoosi F, Mansoori O. Effect of valproic acid in comparison with vorinostat on cell growth inhibition and apoptosis induction in the human colon cancer SW48 cells in vitro. ExpOncol 2018.
13. Sanaei M, Kavoosi F. Effects of 5-aza-2ˈ-deoxycytidine and Valproic Acid on Epigenetic-modifying DNMT1 Gene Expression, Apoptosis Induction and Cell Viability in Hepatocellular Carcinoma WCH-17 cell line. Iran J Ped Hematol Oncol 2019; 2: 83-90.
14. Sanaei M, Kavoosi F. Effect of 5-aza-2'-deoxycytidine in comparison to valproic acid and trichostatin A on histone deacetylase 1, DNA methyltransferase 1, and CIP/KIP family (p21, p27, and p57) genes expression, cell growth inhibition, and apoptosis induction in colon cancer SW480 cell line. Adv Biomed Res 2019; 8: 52-58.
15. Liu J, Li G, Wang X, Wang L, Zhao R, Wang J, et al. Droxinostat, a histone deacetylase inhibitor, induces apoptosis in hepatocellular carcinoma cell lines via activation of the mitochondrial pathway and downregulation of FLIP. Transl Oncol 2016; 9(1): 70-8.
16. Yang W, Zhao X, Pei F, Ji M, Ma W, Wang Y, et al. Activation of the intrinsic apoptosis pathway contributes to the induction of apoptosis in hepatocellular carcinoma cells by valproic acid. Oncol Lett 2015; 9(2): 881-6.
17. Carlisi D, Lauricella M, D’Anneo A, Emanuele S, Angileri L, Di Fazio P, et al. The histone deacetylase inhibitor suberoylanilide hydroxamic acid sensitises human hepatocellular carcinoma cells to TRAIL-induced apoptosis by TRAIL-DISC activation. Eur J Cancer 2009; 45(13): 2425-38.
18. Zhou W, Feng X, Han H, Guo S, Wang G. Synergistic effects of combined treatment with histone deacetylase inhibitor suberoylanilidehydroxamic acid and TRAIL on human breast cancer cells. Sci Rep 2016; 6(1): 1-16.
19. Liu X, Yue P, Khuri FR, Sun S-Y. p53upregulates death receptor 4 expression through an intronic p53 binding site. Cancer Res 2004; 64(15): 5078-83.
20. Soncini M, Santoro F, Gutierrez A, Frigè G, Romanenghi M, Botrugno OA, et al. The DNA demethylating agent decitabine activates the TRAIL pathway and induces apoptosis in acute myeloid leukemia. Biochim Biophys Acta Mol Basis Dis 2013; 1832(1): 114-20.
21. Hasan Z, Ashraf M, Tayyebi A, Hussain R. M. leprae inhibits apoptosis in THP-1 cells by downregulation of Bad and Bak and upregulation of Mcl-1 gene expression. BMC Microbiol 2006; 6(1): 78.
22. Sharifi S, Barar J, Hejazi MS, Samadi N. Doxorubicin changes Bax/Bcl-xL ratio, caspase-8 and 9 in breast cancer cells. Adv Pharm Bull 2015; 5(3): 351.
23. Bolstad AI, Eiken HG, Rosenlund B, Alarcón‐Riquelme ME, Jonsson R. Increased salivary gland tissue expression of Fas, Fas ligand, cytotoxic T lymphocyte–associated antigen 4, and programmed cell death 1 in primary Sjögren's syndrome. Arthritis Rheum 2003; 48(1): 174-85.
24. Fu WN, Bertoni F, Kelsey SM, McElwaine SM, Cotter FE, Newland AC, et al. Role of DNA methylation in the suppression of Apaf-1 protein in human leukaemia. Oncogene 2003; 22(3): 451-5.
25. Rubinek T, Shulman M, Israeli S, Bose S, Avraham A, Zundelevich A, et al. Epigenetic silencing of the tumor suppressor klotho in human breast cancer. Breast Cancer Res Treat 2012; 133(2):6 49-57.
26. Bachman KE, Park BH, Rhee I, Rajagopalan H, Herman JG, Baylin SB, et al. Histone modifications and silencing prior to DNA methylation of a tumor suppressor gene. Cancer Cell 2003; 3(1): 89-95.
27. Sekhavat A, Sun JM, Davie JR. Competitive inhibition of histone deacetylase activity by trichostatin A and butyrate. BCB 2007; 85(6): 751-8.
28. Catalano MG, Fortunati N, Pugliese M, Costantino L, Poli R, Bosco O, et al. Valproic acid induces apoptosis and cell cycle arrest in poorly differentiated thyroid cancer cells. J Clin Endocrinol Metab 2005; 90(3): 1383-9.
29. Gillenwater AM, Zhong M, Lotan R. Histone deacetylase inhibitor suberoylanilidehydroxamic acid induces apoptosis through both mitochondrial and Fas (Cd95) signaling in head and neck squamous carcinoma cells. Mol Cancer Ther 2007; 6(11): 2967-75.
30. Chateauvieux S, Morceau F, Dicato M, Diederich M. Molecular and therapeutic potential and toxicity of valproic acid. BioMed Res Int 2010; 2010.
31. Sasaki K, Yamagata T, Mitani K. Histone deacetylase inhibitors trichostatin A and valproic acid circumvent apoptosis in human leukemic cells expressing the RUNX1 chimera. Cancer Sci 2008; 99(2): 414-22.
32. Sawa H, Murakami H, Ohshima Y, Sugino T, Nakajyo T, Kisanuki T, et al. Histone deacetylase inhibitors such as sodium butyrate and trichostatin A induce apoptosis through an increase of the bcl-2-related protein Bad. Brain Tumor Pathol 2001; 18(2): 109-14.
33. Natoni F, Diolordi L, Santoni C, Montani MSG. Sodium butyrate sensitises human pancreatic cancer cells to both the intrinsic and the extrinsic apoptotic pathways. Biochim Biophys Acta Mol Cell Res 2005; 1745(3): 318-29.
34. Wang L, Luo H, Xia H. Sodium butyrate induces human colon carcinoma HT-29 cell apoptosis through a mitochondrial pathway. J Int Med Res 2009; 37(3): 803-11.
35. Hitomi T, Matsuzaki Y, Yokota T, Takaoka Y, Sakai T. p15INK4b in HDAC inhibitor‐induced growth arrest. FEBS Lett 2003; 554(3): 347-50.
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Sanaei M, Kavoosi F. Effect of valproic acid on extrinsic (DR4, DR5, FAS, FAS-L, TRAIL) and intrinsic (BAX, BAK and APAF1, Bcl-2, and Bcl-xL) apoptotic pathways, cell viability and apoptosis in hepatocellular carcinoma PLC/PRF5 cell line. Feyz Med Sci J 2020; 24 (6) :601-609
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Volume 24, Issue 6 (Bimonthly 2020) Back to browse issues page
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