The G1 phase arrest and apoptosis by intrinsic pathway induced by valproic acid inhibit proliferation of BGC-823 gastric carcinoma cells
详细信息 查看全文
- 作者：Xia Zhao (1)
Weihua Yang (2)
Changwen Shi (1)
Wanshan Ma (1)
Jianing Liu (2)
Yunshan Wang (3)
Guosheng Jiang (2) - 关键词：Histone deacetylase ; Histone deacetylase inhibitor ; BGC ; 823 gastric carcinoma cell ; Valproic acid (VPA) ; Apoptosis
- 刊名：Tumor Biology
- 出版年：2011
- 出版时间：April 2011
- 年：2011
- 卷：32
- 期：2
- 页码：335-346
- 全文大小：905KB
- 参考文献：1. Spotswood HT, Turner BM. An increasingly complex code. J Clin Invest. 2002;110:577鈥?2.
2. Turner BM. Cellular memory and the histone code. Cell. 2002;111:285鈥?1. CrossRef
3. Gray SG, Teh BT. Histone acetylation/deacetylation and cancer: an 鈥渙pen鈥?and 鈥渟hut鈥?case? Curr Mol Med. 2001;1:401鈥?9. CrossRef
4. Marks PA, Rifkind RA, Richon VM, et al. Histone deacetylases and cancer: causes and therapies. Nature. 2001;1:194鈥?02.
5. Satoh A, Toyota M, Itoh F, et al. DNA methylation and histone deacetylation associated with silencing DAP kinase gene expression in colorectal and gastric cancers. Br J Cancer. 2002;86:1817鈥?3. CrossRef
6. Vigushin DM, Coombes RC. Targeted histone deacetylase inhibition for cancer therapy. Curr Cancer Drug Targets. 2004;4(2):205鈥?8. CrossRef
7. Vigushin DM, Coombes RC. Histone deacetylase inhibitors in cancer treatment. Anticancer Drugs. 2002;13:1鈥?3. CrossRef
8. Dokmanovic M, Marks PA. Prospects: histone deacetylase inhibitors. J Cell Biochem. 2005;96:293鈥?04. CrossRef
9. Bird A. Methylation talk between histone and DNA. Science. 2001;294:2113鈥?. CrossRef
10. Aherne GW, Rowlands MG, Stimson L, et al. Assays for the identification and evaluation of histone acetyltransferase inhibitors. Methods. 2002;26:245鈥?3. CrossRef
11. Urnov FD, Wolffe AP. Chromatin remodeling and transcriptional activation: the cast (in order of appearance). Oncogene. 2001;20:2991鈥?006. CrossRef
12. Somech R, Izraelia S, Simon AJ. Histone deacetylase inhibitors: a new tool to treat cancer. Cancer Treat Rev. 2004;30:461鈥?2. CrossRef
13. Yang H, Hoshino K, Sanchez-Gonzalez B, et al. Antileukemia activity of the combination of 5- / aza-2鈥?deoxycytidine with valproic acid. Leuk Res. 2005;29:739鈥?8. CrossRef
14. Cinatl Jr J, Kotchetkov R, Blaheta R, et al. Induction of differentiation and suppression of malignant phenotype of human neuroblastoma BE (2)-C cells by valproic acid: enhancement by combination with interferon-alpha. Int J Oncol. 2002;20:97鈥?06.
15. Moldenhauer A, Frank RC, Pinilla-Ibarz J, et al. Histone deacetylase inhibition improves dendritic cell differentiation of leukemic blasts with AML1-containing fusion proteins. J Leukoc Biol. 2004;76:623鈥?3. CrossRef
16. Kuefer R, Hofer MD, Altug V, et al. Sodium butyrate and tributyrin induce in vivo growth inhibition and apoptosis in human prostate cancer. Br J Cancer. 2004;90:535鈥?1. CrossRef
17. Known SH, Ahn SH, Kim YK, et al. Apicidin, a histone deacetylase inhibitor, induces apoptosis and FAS/FAS ligand expression in human acute promielocytic leukemia cells. J Biol Chem. 2002;277:2073鈥?0. CrossRef
18. Aron JL, Parthun MR, Marucci G, et al. Depsipeptide (FR901228) induces histone acetylation and inhibition of histone deacetylase in chronic lymphocytic leukemia cell concurrent with activation of Caspase 8-mediated apoptosis and downregulation of c-FLIP protein. Blood. 2003;102:652鈥?. CrossRef
19. Chang DW, Xing Z, Capacio VL, et al. Inter-dimer processing mechanism of procaspase-8 activation. EMBO J. 2003;22:4132鈥?2. CrossRef
20. Peart MJ, Tainton KM, Rurefli AA, et al. Novel mechanisms of apoptosis induced by histone deacetylase inhibitors. Cancer Res. 2003;63:4460鈥?1.
21. Pei XY, Dai Y, Grant S, et al. Synergistic induction of oxidative injury and apoptosis in human multiple myeloma cells by the proteasome inhibitor bortezomib and histone deacetylase inhibitors. Clin Cancer Res. 2004;10:3839鈥?2. CrossRef
22. Gao LW, Zhang J, Yang WH, Wang B, Wang JW. Glaucocalyxin A induces apoptosis in human leukemia HL-60 cells through mitochondria-mediated death pathway. Toxicol In Vitro. 2010; [Epub ahead of print]
23. Taunton J, Hassig CA, Schreiber SL. A mammalian histone deacetylase related tothe yeast transc riptional regulator Rpd3p. Science. 1996;272:408鈥?1. CrossRef
24. Abdul M, Hoosein N. Inhibition by anticonvulsants of prostate-specific antigen and interleukin-6 secretion by human prostate cancer cells. Anticancer Res. 2001;21:2045鈥?.
25. Rocchi P, Tonelli R, Camerin C, et al. p21Waf1/Cip1 is a common target induced by short-chain fatty acid HDAC inhibitors (valproic acid, tributyrin and sodium butyrate) in neuroblastoma cells. Oncol Rep. 2005;13:1139鈥?4.
26. Vento R, D鈥橝lessandro N, Giuliano M, et al. Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress. Exp Eye Res. 2000;70:503鈥?7. CrossRef
27. Gozzini A, Rovida E, Sbarba PD, et al. Butyrates, as a single drug, induce histone acetylation and granulocytic maturation: possible selectivity on corebinding factor鈥攁cute myeloid leukemia blasts. Cancer Res. 2003;63:8955鈥?1.
28. Fortunati N, Catalano MG, Arena K, et al. Valproic acid induces the expression of the Na+/I- symporter and iodine uptake in poorly differentiated thyroid cancer cells. J Clin Endocrinol Metab. 2004;82:1006鈥?. CrossRef
29. Luong QT, O鈥橩elly J, Braunstein GD, et al. Antitumor activity of suberoylanilide hydroxamic acid against thyroid cancer cell lines in vitro and in vivo. Clin Cancer Res. 2006;12:5570鈥?. CrossRef
30. Tsou MF, Stearns T. Mechanism limiting centrosome duplication to once per cell cycle. Nature. 2006;442:947鈥?1. CrossRef
31. Catalano MG, Fortunati N, Pugliese M, et al. Valproic acid induces apoptosis and cell cycle arrest in poorly differentiated thyroid cancer cells. J Clin Endocrinol Metab. 2005;90:1383鈥?. CrossRef
32. Zhou Q, He Q, Liang LJ. Expression of p27, Cyclin E and Cyclin A in hepatocellular carcinoma and its clinical significance. World J Gastroenterol. 2003;9:2450鈥?.
33. Macaluso M, Montanari M, Cinti C. Modulation of cell cycle components by epigenetic and genetic events. Semin Oncol. 2005;32:452鈥?. CrossRef
34. Pulukuri SM, Rao JS. Activation of p53/p21Waf1/Cip1 pathway by 5- / aza-2鈥?deoxycytidine inhibits cell proliferation, induces pro-apoptotic genes and mitogen-activated protein kinases in human prostate cancer cells. Int J Oncol. 2005;26:863鈥?1.
35. Gozzini A, Santini V. Butyrates and decitabine cooperate to induce histone acetylation and granulocytic maturation of t(8;21) acute myeloid leukemia blasts. Ann Hematol. 2005;84:54鈥?0. CrossRef
36. Kobayashi H, Tan EM, Fleming SE. Acetylation of histones associated with the p21WAF1/CIP1 gene by butyrate is not sufficient for p21WAF1/CIP1 gene transcription in human colorectal adenocarcinoma cells. Int J Cancer. 2004;109:207鈥?3. CrossRef
37. Park HY, Kim MK, Moon SI, et al. Cell cycle arrest and apoptotic induction in LNCaP cells by MCS-C2, novel cyclin-dependent kinase inhibitor, through p53/p21WAF1/CIP1 pathway. Cancer Sci. 2006;97:430鈥?. CrossRef
38. Nguyen HQ, Selvakumaran M, Liebermann DA, Hoffman B. Blocking c-Myc and Max expression inhibits proliferation and induces differentiation of normal and leukemic myeloid cells. Oncogene. 1995;11:2439鈥?4.
39. Oster SK, Ho CS, Soucie EL, Penn LZ. The Myc oncogene: marvelously complex. Adv Cancer Res. 2002;84:81鈥?54. CrossRef
40. Sommer A, Hilfenhaus S, Menkel A, et al. Cell growth inhibition by the Mad/Max complex through recruitment of histone deacetylase activity. Curr Biol. 1997;7:357鈥?5. CrossRef
41. Hermeking H, Rago C, Schuhmacher M, et al. Identification of CDK4 as a target of c-MYC. Proc Natl Acad Sci USA. 2000;97:2229鈥?4. CrossRef
42. Gustavo L, James D, Rosalie S, Laszlo J, Joseph R. Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F. Nature. 1997;387:422鈥?. CrossRef - 作者单位：Xia Zhao (1)
Weihua Yang (2)
Changwen Shi (1)
Wanshan Ma (1)
Jianing Liu (2)
Yunshan Wang (3)
Guosheng Jiang (2)
1. The Central Laboratory, Qianfoshan Hospital of Shandong Province, Jinan, 250014, China
2. Key Laboratory for Modern Medicine and Technology of Shandong Province, Key Medical Laboratory for Tumor Immunology and Chinese Medicine Immunology of Shandong Province, Key Laboratory for Rare and Uncommon Diseases of Shandong Province, The Institute of Basic Medicine, Shandong Academic of Medical Sciences, Jinan, 250062, China
3. The Central Laboratory, Jinan Central Hospital, Jinan, 250013, China - ISSN：1423-0380
文摘
Recent studies have demonstrated that the histone deacetylation level was closely related to the genesis and development of tumors. Thus, activating histone acetyltransferases and/or suppressing histone deacetylases (HDACs) can become an approach for tumor chemotherapy. The histone acetylation regulation often results in the inhibition of cell proliferation, induction of cell apoptosis or differentiation, and cell cycle arrest in G1 phase. It has been demonstrated recently that the traditional anticonvulsant valproic acid was an efficient class I HDAC inhibitor (HDACI); however, its antitumor effect and mechanisms on gastric cancers so far has not been elucidated clearly. In the present study, gastric carcinoma cell lines BGC-823, HGC-27, and SGC-7901 were cultured with valproic acid (VPA) in vitro. The cell morphology was observed by invert microscope, the proliferation was detected by MTT assay, the apoptosis and cell cycle were analyzed by flow cytometry assay with Annexin V/PI and PI, the activities and protein expressions of Caspase 3, Caspase 8, Caspase 9 of BGC-823 cells were detected by spectrophotometry and indirect immunofluorescence technique, respectively. The protein expressions of Cyclin A, Cyclin D1, Cyclin E, P21Waf/cip1 of BGC-823 cells were analyzed by indirect immunofluorescence assay, and messenger ribonucleic acid (mRNA) expressions were detected by RT-PCR assay. The results showed that the proliferation of three kinds of gastric carcinoma cells could be inhibited obviously by VPA, which was related to the apoptosis induction and cell cycle arrest in G1 phase. The intrinsic pathway (cytochrome C pathway) was chiefly involved in the mechanism of apoptosis, which was indicated by activation of Caspase 9 and Caspase 3. The extrinsic pathway was partially involved, with slight activation of Caspase 8. The mechanism underlying its effect on cell cycle arrest in G1 phase induction was due to the upregulation of P21Waf/cip1, Mad1 expression and downregulation of Cyclin A, c-Myc expression.