ABSTRACT
<p><b>OBJECTIVE</b>To examine the effects of sodium phenylbutyrate on the apoptosis of human tongue squamous cancer cell line and expression of p21 and survivin genes.</p><p><b>METHODS</b>The inhibition effects of sodium phenylbutyrate on Tca8113 and human tongue squamous cell carcinoma (TCSSA) cell lines were detected by methyl thiazoly terazolium (MTT) and the apoptosis of the cancer cells after being induced by sodium phenylbutyrate examined by flow cytometry (FCM). The expression of p21 and survivin genes were observed with Western blotting and RT-PCR.</p><p><b>RESULTS</b>Compared with control group, the level of p21 mRNA and protein of Tca8113 cellline increased to 0.09 ± 0.08 and increased 0.72 ± 0.10, that of TCSSA cellline increased 1.34 ± 0.12 and 1.56 ± 0.09 (P < 0.05). Compared with control group, the level of surrive mRNA and protein of Tca8113 cellline decreased to 1.10 ± 0.05 and 1.14 ± 1.10, that of TCSSA cellline decreased to 0.12 ± 0.08 and 0.94 ± 0.09 (P < 0.05). Sodium phenylbutyrate inhibited the cell proliferation, promoted cell apoptosis and arrested the cells in G₁/G₀ phase. The amount of p21 mRNA and protein were increased, and the expression of survivin gene was decreased.</p><p><b>CONCLUSIONS</b>Sodium phenylbutyrate exhibited remarkable inhibitory effects on human tongue squamous cancer cell proliferation and induced cancer cell apoptosis. The mechanism may be due to up-regulation of p21 gene and down-regulation of survivin gene. The mRNA level of p21 gene and survivin gene showed a strong correlation.</p>
Subject(s)
Humans , Apoptosis , Cell Line, Tumor , Cell Proliferation , Cyclin-Dependent Kinase Inhibitor p21 , Metabolism , Inhibitor of Apoptosis Proteins , Metabolism , Neoplasms, Squamous Cell , Pathology , Phenylbutyrates , Pharmacology , Tongue Neoplasms , PathologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of tumor necrosis factor alpha (TNFalpha) on radiosensitivity of nasopharyngeal carcinoma (NPC) in relation to TNFalpha-induced cell cycle synchronization.</p><p><b>METHODS</b>The radio-resistance of a NPC cell line subclone CNE-2Z-S1 was verified by in vivo experiments and flow cytometry was performed to evaluate cell cycle synchronization in TNFalpha-treated CNE-2Z-S1 cells. The radiosensitivity of the cell synchronized CNE-2Z-S1 cells was determined by clone formation in vitro and in vivo experiment in nude mice.</p><p><b>RESULTS</b>TNFalpha was capable of inducing cell cycle arrest and synchronization of CNE-2Z-S1 cells. Pretreatment with TNFalpha remarkably enhanced the radiosensitivity of CNE-2Z-S1 in vitro, and in vivo experiments with nude mice also suggested the role of TNFalpha in enhancing the radiosensitivity of NPC.</p><p><b>CONCLUSION</b>TNFalpha can enhance the radiosensitivity of NPC cells by inducing cell cycle synchronization.</p>