Trichostatin A, a histone deacetylase inhibitor, suppresses proliferation and promotes apoptosis of esophageal squamous cell lines

Molecular Medicine Reports

Volumn 11, Issue 6, 2015, Pages 4525-4531

  Ma, Junfen ^a   Guo, Xiaobing ^a   Zhang, Shijie ^a   Liu, Hongchun ^a   Lu, Jing ^b   Dong, Ziming ^b   Liu, Kangdong ^b   Ming, Liang ^a  

^a THE FIRST AFFILIATED HOSPITAL OF ZHENGZHOU UNIVERSITY   (China)

^b ZHENGZHOU UNIVERSITY   (China)

Author keywords

Apoptosis; Esophageal squamous cell carcinoma; Histone deacetylase inhibitor; Trichostatin A

Indexed keywords

GELATINASE A; GELATINASE B; HELENALIN; MATRINE; PROTEIN P50; SYNAPTOTAGMIN I; CYCLIN DEPENDENT KINASE INHIBITOR 1A; CYCLIN DEPENDENT KINASE INHIBITOR 1B; HISTONE; HISTONE DEACETYLASE INHIBITOR; HYDROXAMIC ACID; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN BAX; PROTEIN BCL 2; PROTEIN KINASE B; TRICHOSTATIN A;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIPROLIFERATIVE ACTIVITY; ARTICLE; CANCER INHIBITION; CARCINOMA CELL; CELL INVASION; CELL MIGRATION; CELL PROLIFERATION; CELL VIABILITY; CONTROLLED STUDY; HUMAN; HUMAN CELL; MALE; METASTASIS INHIBITION; MOUSE; NASOPHARYNX CARCINOMA; NONHUMAN; PROTEIN EXPRESSION; XENOGRAFT; ACETYLATION; APOPTOSIS; DRUG EFFECTS; ESOPHAGUS TUMOR; G1 PHASE CELL CYCLE CHECKPOINT; METABOLISM; PATHOLOGY; PHOSPHORYLATION; SQUAMOUS CELL CARCINOMA; TUMOR CELL LINE;

ACETYLATION; APOPTOSIS; BCL-2-ASSOCIATED X PROTEIN; CARCINOMA, SQUAMOUS CELL; CELL LINE, TUMOR; CELL PROLIFERATION; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLIN-DEPENDENT KINASE INHIBITOR P27; ESOPHAGEAL NEOPLASMS; G1 PHASE CELL CYCLE CHECKPOINTS; HISTONE DEACETYLASE INHIBITORS; HISTONES; HUMANS; HYDROXAMIC ACIDS; MITOGEN-ACTIVATED PROTEIN KINASE 1; MITOGEN-ACTIVATED PROTEIN KINASE 3; PHOSPHATIDYLINOSITOL 3-KINASES; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; PROTO-ONCOGENE PROTEINS C-BCL-2;

EID: 84924709760     PISSN: 17912997     EISSN: 17913004     Source Type: Journal    
DOI: 10.3892/mmr.2015.3268     Document Type: Article

References (37)

1. Zhu H, Huo X, Chen L, Wang H and Yu H: Clinical experience with radio-, chemo-and hyperthermotherapy combined trimodality on locally advanced esophageal cancer. Mol Clin Oncol 1: 1009-1012, 2013.
2. Jemal A, Center MM, DeSantis C and Ward EM: Global patterns of cancer incidence and mortality rates and trends. Cancer Epidemiol Biomarkers Prev 19: 1893-1907, 2010.
3. Minsky BD, Pajak TF, Ginsberg RJ, et al: INT 0123 (Radiation Therapy Oncology Group 94-05) phase III trial of combined-modality therapy for esophageal cancer: high-dose versus standard-dose radiation therapy. J Clin Oncol 20: 1167-1174, 2002.
4. Minucci S and Pelicci PG: Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer. Nat Rev Cancer 6: 38-51, 2006.
5. Reichert N, Choukrallah MA and Matthias P: Multiple roles of class I HDACs in proliferation, differentiation and development. Cell Mol Life Sci 69: 2173-2187, 2012.
6. Ellis L, Atadja PW and Johnstone RW: Epigenetics in cancer: targeting chromatin modifications. Mol Cancer Ther 8: 1409-1420, 2009.
7. Ellis L and Pili R: Histone deacetylase inhibitors: advancing therapeutic strategies in hematological and solid malignancies. Pharmaceuticals (Basel) 3: 2411-2469, 2010.
8. Abbas A and Gupta S: The role of histone deacetylases in prostate cancer. Epigenetics 3: 300-309, 2008.
9. Bonfils C, Walkinshaw DR, Besterman JM, Yang XJ and Li Z: Pharmacological inhibition of histone deacetylases for the treatment of cancer, neurodegenerative disorders and inflammatory diseases. Expert Opin Drug Discov 3: 1041-1065, 2008.
10. Ropero S and Esteller M: The role of histone deacetylases (HDACs) in human cancer. Mol Oncol 1: 19-25, 2007.
11. Cress WD and Seto E: Histone deacetylases, transcriptional control and cancer. J Cell Physiol 184: 1-16, 2000.
12. Meng F, Sun G, Zhong M, Yu Y and Brewer MA: Inhibition of DNA methyltransferases, histone deacetylases and lysine-specific demethylase-1 suppresses the tumorigenicity of the ovarian cancer ascites cell line SKOV3. Int J Oncol 43: 495-502, 2013.
13. Ueki N, Lee S, Sampson NS and Hayman MJ: Selective cancer targeting with prodrugs activated by histone deacetylases and a tumour-associated protease. Nat Commun 4: 2735, 2013.
14. Wilson PM, Labonte MJ, Martin SC, et al: Sustained inhibition of deacetylases is required for the antitumor activity of the histone deactylase inhibitors panobinostat and vorinostat in models of colorectal cancer. Invest New Drugs 31: 845-857, 2013.
15. Chen X, Xiao W, Chen W, Luo L, Ye S and Liu Y: The epigenetic modifier trichostatin A, a histone deacetylase inhibitor, suppresses proliferation and epithelial-mesenchymal transition of lens epithelial cells. Cell Death Dis 4: e884, 2013.
16. Stein C, Riedl S, Rüthnick D, Nötzold RR and Bauer UM: The arginine methyltransferase PRMT6 regulates cell proliferation and senescence through transcriptional repression of tumor suppressor genes. Nucleic Acids Res 40: 9522-9533, 2012.
17. Cai Y, Cui W, Chen W, et al: The effects of a histone deacetylase inhibitor on biological behavior of diffuse large B-cell lymphoma cell lines and insights into the underlying mechanisms. Cancer Cell Int 13: 57, 2013.
18. Spiegel S, Milstien S and Grant S: Endogenous modulators and pharmacological inhibitors of histone deacetylases in cancer therapy. Oncogene 31: 537-551, 2012.
19. Mutze K, Langer R, Becker K, et al: Histone deacetylase (HDAC) 1 and 2 expression and chemotherapy in gastric cancer. Ann Surg Oncol 17: 3336-3343, 2010.
20. Jurkin J, Zupkovitz G, Lagger S, et al: Distinct and redundant functions of histone deacetylases HDAC1 and HDAC2 in proliferation and tumorigenesis. Cell Cycle 10: 406-412, 2011.
21. Hoshino I and Matsubara H: Recent advances in histone deacetylase targeted cancer therapy. Surg Today 40: 809-815, 2010.
22. Noureen N, Rashid H and Kalsoom S: Identification of type-specific anticancer histone deacetylase inhibitors: road to success. Cancer Chemother Pharmacol 66: 625-633, 2010.
23. Marson CM: Histone deacetylase inhibitors: design, structure-activity relationships and therapeutic implications for cancer. Anticancer Agents Med Chem 9: 661-692, 2009.
24. Rezaei PF, Fouladdel S, Hassani S, et al: Induction of apoptosis and cell cycle arrest by pericarp polyphenol-rich extract of Baneh in human colon carcinoma HT29 cells. Food Chem Toxicol 50: 1054-1059, 2012.
25. Ward CS, Eriksson P, Izquierdo-Garcia JL, Brandes AH and Ronen SM: HDAC inhibition induces increased choline uptake and elevated phosphocholine levels in MCF7 breast cancer cells. PLoS One 8: e62610, 2013.
26. Watson JA, McKenna DJ, Maxwell P, et al: Hyperacetylation in prostate cancer induces cell cycle aberrations, chromatin reorganization and altered gene expression profiles. J Cell Mol Med 14: 1668-1682, 2010.
27. Gerard C and Goldbeter A: From quiescence to proliferation: Cdk oscillations drive the mammalian cell cycle. Front Physiol 3: 413, 2012.
28. Yagi Y, Fushida S, Harada S, et al: Effects of valproic acid on the cell cycle and apoptosis through acetylation of histone and tubulin in a scirrhous gastric cancer cell line. J Exp Clin Cancer Res 29: 149, 2010.
29. Wang C, Fu M, Mani S, Wadler S, Senderowicz AM and Pestell RG: Histone acetylation and the cell-cycle in cancer. Front Biosci 6: D610-D629, 2001.
30. Aguero MF, Facchinetti MM, Sheleg Z and Senderowicz AM: Phenoxodiol, a novel isoflavone, induces G1 arrest by specific loss in cyclin-dependent kinase 2 activity by p53-independent induction of p21WAF1/CIP1. Cancer Res 65: 3364-3373, 2005.
31. Queiroz AB, Focchi G, Dobo C, Gomes TS, Ribeiro DA and Oshima CT: Expression of p27, p21 (WAF/Cip1) and p16 (INK4a) in normal oral epithelium, oral squamous papilloma and oral squamous cell carcinoma. Anticancer Res 30: 2799-2803, 2010.
32. Tula-Sanchez AA, Havas AP, Alonge PJ, et al: A model of sensitivity and resistance to histone deacetylase inhibitors in diffuse large B cell lymphoma: Role of cyclin-dependent kinase inhibitors. Cancer Biol Ther 14: 949-961, 2013.
33. You BR and Park WH: Trichostatin A induces apoptotic cell death of HeLa cells in a Bcl-2 and oxidative stress-dependent manner. Int J Oncol 42: 359-366, 2013.
34. Hacker S, Karl S, Mader I, et al: Histone deacetylase inhibitors prime medulloblastoma cells for chemotherapy-induced apoptosis by enhancing p53-dependent Bax activation. Oncogene 30: 2275-2281, 2011.
35. Zhang J, Roberts TM and Shivdasani RA: Targeting PI3K signaling as a therapeutic approach for colorectal cancer. Gastroenterology 141: 50-61, 2011.
36. Chen CS, Weng SC, Tseng PH, Lin HP and Chen CS: Histone acetylation-independent effect of histone deacetylase inhibitors on Akt through the reshuffling of protein phosphatase 1 complexes. J Biol Chem 280: 38879-38887, 2005.
37. Liu B and Kuang A: Genetic alterations in MAPK and PI3K/Akt signaling pathways and the generation, progression, diagnosis and therapy of thyroid cancer. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi 29: 1221-1225, 2012 (In Chinese).