Role of Survivin gene on the apoptosis of adenoid cystic carcinoma-2 cells induced by arsenic trioxide / 华西口腔医学杂志

<p><b>OBJECTIVE</b>To investigate the proliferation effects of arsenic trioxide (As2O3) on salivary adenoid cystic carcinoma-2 (ACC-2) cells in vitro and to study the role of Survivin on the apoptosis of ACC-2 induced by As2O3.</p><p><b>METHODS</b>ACC-2 cells were treated with different concentration of As2O3 for different time. The inhibitory effects on cell's viability were assayed with methyl thiazolyl tetrazolium (MTT) test. Apoptosis was determined by flow cytometry. The expression of Survivin mRNA and protein were investigated by reverse transcription-polymerase chain raction (RT-PCR) and Western blot analysis respectively.</p><p><b>RESULTS</b>Cell viability after As2O3 treatment was markedly suppressed and exhibited as a dose- and time-dependent pattern. The apoptotic index showed the similar trend. The results of RT-PCR revealed gene expression of Survivin was suppressed significantly. Through Western blot analysis, a negative correlation between concentration and amount of protein product of Survivin was determined.</p><p><b>CONCLUSION</b>As2O3 might markedly suppressed ACC-2 cell's viability in vitro. The inhibition of Survivin gene expression may play a critical role on ACC-2 cell apoptosis induced by As2O3.</p>

Inhibitory effect of transforming growth factor-β(1) on oral squamous cell carcinoma brain metastasis Tb cell line / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To investigate the inhibitory effect of transforming growth factor (TGF)-β₁ on oral squamous cell carcinoma (OSCC) Tb cell line.</p><p><b>METHODS</b>Cell counting method was used to examine the inhibitory effect of TGF-β₁ on Tb cell and flow cytometry (FCM) assay performed to measure the changes of cell cycle. Superarray was used to screen the changing expression of genes in TGF-β₁/Smads signaling pathway.RT-PCR method was used to detect the results of Superarray.</p><p><b>RESULTS</b>TGF-β₁ showed significant inhibiting effect on OSCC Tb cell line. TGF-β₁ blocked the cell cycle at G₁ phase. The expression level of activin receptor-like kinase-1 (ACVRL-1), anti-mullerian hirmine (AMH), cyclim-dependent kinase inhibitor-2B (CDKN-2B) and transforming growth factor-beta-indnced factor (TGIF) was higer in the cells treated with TGF-β₁ than in control, while TDGF-1 expression was down-regulated. ACVRL-1 and CDKN-2B gene expression was consistent with the results of Superarray.</p><p><b>CONCLUSIONS</b>TGF-β₁ can inhibit the growth of OSCC Tb cell line. The mechanism may be related to the regulation of cell cycle and the expression of ACVRL-1 and CDKN-2B in TGF-β₁-Smads signaling pathway.</p>

Functional significance of TGF-beta1 signal transduction pathway in oral squamous cell carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>The aim of this study was to investigate the expression of transforming growth factor-beta1 (TGF-beta1) and its signaling pathway molecules in oral squamous cell carcinoma (OSCC) and analyze the association between these factors and genesis and metastasis of OSCC.</p><p><b>METHODS</b>The express of TGF-beta1, TbetaRI, TbetaRII and Smad4, a pivotal downstream molecule of its signaling, in 10 normal oral mucosa tissues and 108 OSCC was detected by SP immunohistochemistry, and thier correlation with genesis and metastasis of OSCC were assessed.</p><p><b>RESULTS</b>The expressions of TbetaRII and Smad4 were lower in the tumors (34.3%, 38.9%) than those in the normal oral epithelium (80.0%, 100.0%, P < 0.05). The positive expression rates of TGF-beta1 and TbetaRI in the normal oral epithelium and OSCC were not significantly different (P > 0.05). There was an inverse correlation between TGF-beta1, Smad4, TbetaRII, TbetaRI expression and clinical stages (P < 0.01). The expression of TGF-beta1 was related with histological differentiation and tumor localization (P < 0.05). There was a relationship beteween Smad4 expression and histological differentiation and lymph node metastasis (P < 0.05). The expression of TbetaRII in the samples with lymph node metastasis was less than that in the ones without lymph node metastasis (P < 0.01), although there was no association between expression of TbetaRII and lymph node metastasis status.</p><p><b>CONCLUSION</b>There is an important relationship between the abnormal TGF-beta1/Smad4 signal pathway and genesis and development of OSCC, while the low expressed Smad4 and TbetaRII may promote the metastasis of OSCC.</p>