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曲古抑菌素A对舌鳞癌SCC-6细胞生物学行为的影响 被引量:1

Effects of TSA on Cell Growth,Cell Cycle,Apoptosis and Invasion of Tongue Squamous Cell Carcinoma SCC-6 Cell Line in vitro
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摘要 目的:观察曲古抑菌素A(TSA)对舌鳞癌细胞生物学行为的影响,探讨其体外抗癌活性。方法:不同浓度、时间梯度TSA处理人舌鳞癌SCC-6细胞后,MTT法检测细胞增殖活性;流式细胞仪定量检测细胞周期和凋亡变化;Transwell法测定细胞体外侵袭性改变。结果:①TSA对SCC-6细胞的增殖有明显抑制作用,并呈剂量和时间依赖性;②随着TSA浓度的增加,SCC-6细胞G1期的细胞数目逐渐减少,而S期和G2/M期的细胞数目增加,提示TSA将细胞周期抑制在S期和G2/M期,同时随着TSA浓度的增加,SCC-6细胞的凋亡率与对照组相比明显增加(P<0.05),提示TSA能促进SCC-6细胞的凋亡;③经不同浓度TSA处理24 h后,SCC-6细胞穿透人工基质膜的细胞数随着TSA浓度上升而逐渐减小,提示TSA能显著抑制SCC-6细胞的侵袭性。结论:体外条件下,TSA能明显抑制SCC-6细胞的增殖和侵袭能力,诱导其凋亡。而其所介导的细胞凋亡很可能与S期和G2/M期细胞周期的阻滞有关。 Objective: This study was aimed to investigate weather trichostatin A can affect cell growth, apoptosis, cell cycle, and invasiveness of tongue squamous cell carcinoma SCC-6 cell line in vitro, which reveals the anticancer activities. Methods: SCC-6 cells were treated with TSA in different concentrations with various time intervals in vitro. Proliferative activities of these cells were assessed by MTT assay. Cell cycle and cell apoptosis were analyzed by flow cytometry using Annexin V, and invasive properties were detected by Transwell ways. Results: TSA inhibited the proliferation of SCC-6 cells in a dose- and time-dependent manner. TSA arrested the cell cycle in G2/M phase with the decreasing amount of G2 phase and the increasing of S and G2/M phase. The apoptosis rate increased gradually in dose- and time-dependent manner, which showed significant difference comparing with control group (P〈0.05). TSA inhibited the invasion rate of SCC-6 cells at different concentrations (P〈0.05). Conclusion: In vitro, TSA shows potential on anticancer activities, inhibits SCC-6 cells proliferation and invasion, arrests the cell cycle in G2/M phase which induces cell apoptosis.
出处 《口腔颌面外科杂志》 CAS 2011年第4期242-246,共5页 Journal of Oral and Maxillofacial Surgery
基金 上海市科学技术委员会青年科技启明星计划项目(09QA1406400)
关键词 曲古抑菌素A 舌鳞癌 增殖 细胞周期 凋亡 侵袭性 体外实验 trichostatin A (TSA) tongue squamous cell carcinoma proliferation cell cycle apoptosis invasion in vitro
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参考文献12

  • 1Puppin C, Passon N, Franzoni A, et al. Histone deacetylase inhibitors control the transcription and alternative splicing of prohibitin in thyroid tumor cells.[J]. Oncol Rep,2011,25(2):393-397.
  • 2Yoshida M, Kijima M, Akita M, et al. Potent and specific inhibition of mammalian histone deacetylase both in vivo and in vitro by trichostatin A[J]. J Biol Chem,1990,265(28): 17174-17179.
  • 3Kwon HJ, Kim MS, Kim MJ, et al. Histone deacetylase inhibitor FK228 inhibits tumor angiogenesis [J]. Int J Cancer, 2002, 97(3):290-296.
  • 4Vigushin DM, Ali S, Pace PE, et al. Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer in vivo [J]. Clin Cancer Res, 2001,7 (4):971-976.
  • 5Marks P, Rifkind RA, Richon VM, et al. Histone deacetylases and cancer : causes and therapies[J]. Nat Rev Cancer, 20013(3):194-202.
  • 6Liu LT, Chang HC, Chiang LC, et al. Histone deacetylase inhibitor up-regulates RECK to inhibit MMP-2 activation and cancer cell invasion[J]. Cancer Res, 2003,63(12):3069- 3072.
  • 7Papeleu P, Loyer P, Vanhaecke T, et al. Trichostatin A induces differential cell cycle arrests but does not induce apoptosis in primary cultures of mitogen-stimulated rat hepatocytes[J]. J Hepatol, 2003,39(3):374-382.
  • 8Monneret C. Histone deacetylase inhibitors [J]. Eur J Med Chem, 2005,40(1):1-13.
  • 9Li L, Shi HD, Yiannoutsos C, et al. Epigonetic hypothesis tests for methylation and acatylation in a triple microarray systerm[J]. Comput Biol, 2005,12(3):370-390.
  • 10Kim YB, Ki SW, Yoshida M, et al. Mechanism of cell cycle arrest caused by histone deacetylase inhibitors in human carcinoma cells[J]. J Antibiot(Tokyo), 2000,53(10): 1191-1200.

二级参考文献46

  • 1Parkin DM,Pisani P,Ferlay J.Global cancer statistics[J].CA Cancer J Clin,1999,49(1):33-64.
  • 2Landis SH,Murray T,Bolden S,et al.Cancer statics,1999[J].CA Cancer J Clin,1999,49(1):8-31.
  • 3Goymer P.Natural selection:the evolution of cancer[J].Nature,2008,454(7208):1046-1048.
  • 4Merlo LM,Pepper JW,Beid BJ,et al.Cancer as an evolutionary and ecological process[J].Nat Bev Cancer,2006,6(12):924-935.
  • 5Gupta GP,Massagne J.Cancer metastasis:building a framework[J].Cell,2006,127(4):679-695.
  • 6Wang X,Zhang J,Fan M,et al.The expression of Ecadherin at the invasive tumor front of oral squamous cell carcinoma:immunohistochemieal and RT-PCR analysis with clinicopathologieal correlation[J].Oral Surg Oral Med Oral Pathol Oral Radiol Endod,2009,107(4):547-554.
  • 7Wheeloek M J,Shintani Y,Maeda M,et al.Cadherin switching[J].J Cell Sci,2008,121(Pt 6):727-735.
  • 8de Moraes RV,Oliveira DT,Landman G,et al.E-cadherin abnormalities resulting from CPG methylation promoter in metastatic and nonmetastatic oral cancer[J].Head Neck,2008,30(1):85-92.
  • 9Nakayama S,Sasaki A,Mesc H,et al.The E-cadherin gene is silenced by CpG methylation in human oral squamous cell carcinomas[J].Int J Cancer,2001,93(5):667-673.
  • 10Acloque H,Adams MS,Fishwick K,et al.Epithelialmesenchymal transitions:the importance of changing cell state in development and disease[J].J Clin Invest,2009,119(6):1438-1449.

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  • 1Richard DE, Berra E, Pouyssegur J. Angiogenesis: how a tumor adapts to hypoxia [J]. Biochem Biophys Res Commun,1999, 266(3):718-722.
  • 2Hockel M, Schlenger K, Mitze M, et al. Hypoxia and radiation response in human tumors [J]. Semin Radiat 0nco1,1996, 6(1):3-9.
  • 3Vigushin DM, All S, Pace PE, et al. Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer in vivo [J]. Clin Cancer Res,2001,7 (4):971-976.
  • 4Hillen F,Griffioen AW.Tumour vascularization:sprouting angiogenesis and beyond [J]. Cancer Metastasis Rev, 2007,26 (3-4):489-502.
  • 5Semenza GL. Expression of hypoxia-inducible factor 1: mechanisms and consequences [J]. Biochem Pharmacol, 2000,59(1):47-53.
  • 6Semenza GL. HIF-I: mediator of physiological and pathophysiological responses to hypoxia [J]. J Appl Physiol,2000,88(4): 1474-1480.
  • 7Krishnamachary B, Berg-Dixon S, Kelly B, et al. Regulation of colon carcinoma cell invasion by hypoxia- inducible factor 1 [J]. Cancer Res,2003,63(5):1138-1143.
  • 8Ryan HE, Poloni M, McNulty W, et al. Hypoxia-inducible factor-lalpha is a positive factor in solid tumor growth [J]. Cancer Res,2000,60(15):4010-4015.
  • 9Kim MS, Kwon HJ, Lee YM, et al. Histone deacetylases induce angiogenesis by negative regulation of tumor suppressor genes [J]. Nat Med,2001,7(4):437-443.
  • 10Williams RJ. Trichostatin A, an inhibitor of histone deacetylase, inhibits hypoxia-induced angiogenesis [J]. Expert Opin Investig Drugs,2001,10(8): 1571-1573.

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