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@#[Abstract] Objective: To detect the expression of miR-126 in oral squamous cell carcinoma (OSCC) and to analyze its correlation with clinicopathological features and prognosis of patients, as well as to explore the effect of miR-126 over-expression on the malignant biological behaviors of Tca8113 cells. Methods: A total of 62 pairs of cancer and para-cancerous tissue specimens from OSCC patients who were surgically treated in the First Affiliated Hospital of Zhengzhou University from June 2016 to June 2018 were collected for this study; in addition, human tongue squamous carcinoma Tca8113 cell line and human mouth keratinocyte HOK cell line were also selected for this study. The expression of miR-126 in cancer tissues and cells was detected by qPCR, and the relationship between miR-126 expression and clinicopathological features and prognosis of the patients was analyzed. miR-126 mimics and miR-NC plasmids were respectively transfected into Tca8113 cells by liposome transfection technology. Cell proliferation, apoptosis, migration and invasion were detected by MTT method, Flow cytometry and Transwell chamber method, respectively; and the expressions of apoptosis, migration and invasion related proteins were detected by Western blotting. Results: The expression level of miR-126 in OSCC tissues and Tca8113 cells was significantly lower than that in para-cancerous tissues and HOK cells (all P<0.01). The expression of miR-126 was associated with TNM stage and lymph node metastasis (all P<0.05), and patients with high miR-126 expression had significantly better overall survival rate than patients with low expression (P<0.05). After transfection with miR-126 mimics, the cell proliferation, migration and invasion ability significantly decreased (P<0.05 or P<0.01) while the apoptosis rate significantly increased in Tca8113 cells (P<0.01), the expression levels of Bcl-2, N-cadherin and vimentin in Tca8113 cells significantly decreased (all P<0.01), and expression levels of Bax and E-cadherin significantly increased (all P<0.01). Conclusion: miR-126 is low expressed in OSCC tissues and Tca8113 cells. Up-regulation of miR-126 inhibits cell proliferation, migration and invasion and promotes apoptosis of Tca8113 cells.
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Objective To investigate the effects of osthole on the proliferation,apoptosis,and autophagy of human tongue cancer Tca8113 cells and explore its possible mechanism of action. Methods Tca8113 cells were cultured
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Humans , Apoptosis , Autophagy , Cell Line, Tumor , Cell Proliferation , Coumarins , Tongue NeoplasmsABSTRACT
AIM: To investigate the effect of endoplasmic reticulum stress pathway on the apoptosis of tongue squamous cancer Tca8113 cells induced by antitumor component-I from Agkistrodon acutus venom (AAVC-I). METHODS: The in vitro experiments were performed on subculture tongue squamous cancer Tca8113 cells in their growth period. A normal control group, a DL-dithiothreitol (DTT) positive control group and different AAVC-I concentrations were set according to the experiment objective. MTT assay was used to detect the proliferation inhibition of Tca8113 cells after been treated with different concentrations of DTT and AAVC-I for 24 h. The results were used to choose appropriate concentrations of DTT and AAVC-I in DTT positive control group and AAVC-I treated group, respectively. HE staining and Annexin V-FITC/PI double fluorescence staining were used to monitor the apoptosis of Tca8113 cells. Western blot was used to identify the expression levels of apoptosis-related proteins including endoplasmic reticulum stress glucose-regulatory protein 78 (GRP78), enhance-binding protein-homologousprotein (CHOP), cysteine-containing aspartate specific protease-12 (Caspase-12), cysteine-containing aspartate specific protease-9 (Caspase-9) and cysteine-containing aspartate specific protease-3 (Caspase-3).RESULTS:The proliferation inhibition of Tca8113 cells increased with an increased concentration of AAVC-I concentration (P<0.05), causing cell shrinkage, increased cell gaps, cytonuclear condensation, cell fragmentation, the appearance of apoptotic bodies, and increased rate of apoptosis (P<0.05). In addition, the expression level of GRP78 protein, CHOP protein, proteins of Caspase-12, Caspase-9 and Caspase-3 were increased (P<0.05).CONCLUSION: Endoplasmic reticulum stress CHOP/Caspase-12 pathway plays an important role in AAVC-I induced Tca8113 cells apoptosis.
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Aim To investigate the effect of asiatic acid(AA) on the proliferation, apoptosis and cell cycle arrest of human tongue carcinoma TCA-8113 cells, and the possible mechanism. Methods The inhibitory effect of AA(0, 20, 30, 40, 50 pjnol • L"1) at different concentrations on TCA-8113 cells for 24 h was determined by MTT. The effect of AA on the colony formation rate of TCA-8113 cells was detected by colony formation test; The apoptosis of TCA-8113 cells by AA was detected by Hoechst 33342 staining and Annexin V-FITC/PI staining. Cell cycle changes were analyzed by flow cytometry. The expressions of protein in human tongue cancer cells, such as bcl-2, Bax, cleaved caspase-3, p53 and p21 proteins were detected by Western blot. Results The inhibitory rate of AA on TCA-8113 cells was concentration-dependent (P < 0.05), with the IC50 concentration of 42. 13 (xmol • L- 1, and the ability of cell colony formation decreased. The apoptosis rate increased with the increase of AA concentration (P < 0. 05). The concentration of AA 30 u.mol -L"1 gradually blocked the cell cycle in G2/M phase. Western blot analysis showed that the expressions of p53, p21 and Bax increased, while Bcl-2 decreased in a dose-dependent effect (P<0. 05). Conclusions AA can significantly inhibit the proliferation and apoptosis of human tongue carcinoma TCA-8113 cells, and its mechanism may be related to the regulation of p53 pathway related proteins p53, p21, Bax and the inhibition of Bcl-2 expression, and AA can arrest TCA-8113 cells cycle in G2/M phase.
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@# Objective: To investigate the molecular mechanisms of lncRNA XIST/miR-34a-5p/SIRT6 axis regulating the proliferation and metastasis of oral squamous cell carcinoma (OSCC) cells. Methods: Specimens of tumor tissues and paracancer tissues of 47 patients with OSCC, who visited the Qingdao Stomatological Hospital from March 2013 to March 2018, were enrolled in this study. qPCR was performed to measure the mRNA expressions of lncRNA XIST, miR-34a-5p and SIRT6 in OSCC tissues and cell lines. WB was performed to measure the protein levels of SIRT6, Ki67, pcDNA, cleaved-caspase3, cleaved-caspase8, E-cadherin and vimentin in OSCC tissues and cell lines. CCK-8 assay was performed to observe the effect of lncRNA XIST knockdown on proliferation of Cal-27 and Tca-8113 cells; Tanswell assay was performed to detect migration and invasion of Cal-27 and Tca-8113 cells; flow cytometry was performed to detect the apoptosis of Cal-27 and Tca-8113 cells; and dual luciferase reporter assay was performed to verify the relationship between lncRNAXIST and miR-34a, or miR-34a and SIRT6. Results: Expressions of lncRNAXIST and SIRT6 were up-regulated in OSCC tissues and cell lines (all P<0.05), reversely, miR-34a-5p was down-regulated in OSCC tissues and cell lines (P<0.01). lncRNA XIST knockdown significantly suppressed OSCC cells proliferation, migration and invasion, and induced apoptosis of OSCC cells (all P<0.01); however, simultaneous transfection with miR-34a-5p inhibitor or pcDNA-SIRT6 vector exerted opposite effect. lncRNA XIST knockdown significantly increased cell proliferation and metastasis related protein expression in OSCC cells (all P< 0.01), and simultaneous transfection with miR-34a-5p inhibitor or pcDNA-SIRT6 vector exerted opposite effect. In addition, lncRNA XIST directly targeted miR-34a-5p, and miR-34a-5p targeted SIRT6, lncRNA XIST upregulated SIRT6 expression via inhibiting miR34a-5p (P<0.01). Conclusion: Taken together, lncRNA XIST/miR-34a-5p/SIRT6 axis regulates the proliferation and metastasis of OSCC cells and provides potential therapeutic targets for OSCC.
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Objective: To analyze the changes of gene profile of over-expression WWOX gene in the human oral squamous cell carcinoma (OSCC) Tca8113 cells, and to explore the tumor inhibition mechanism of WWOX gene. Methods: The Tca8113 cells were divided into WWOX over-expression group and control group. In WWOX over-expression group, the lentiviral plasmid carrying the full-length cDNA fragment of WWOX gene was infected into the Tca8113 cells, while in control group, the lentiviral plasmid carrying the empty pGV287-LV vector was infected into the Tca8113 cells. The quantitative real time PCR (qRT-PCR) and Western blotting methods were used to detect the expressions of WWOX mRNA and protein. The gene chip technique was used to screen the differientially expressed genes and biological analysis was performed. The quantitative PCR was used to detect the relative mRNA expression levels of differientially expressed genes involving in the mitogen-activated protein kinase (MAPK) signaling pathway. Results: After infection, the relative mRNA expression level of WWOX gene in the Tca8113 cells in WWOX over-expression group was higher than that in control group (P<0. 05), and the expression of WWOX protein in the Tca8113 cells in WWOX over-expression group was higher. A total of 347 differientially expressed genes with a 1. 5-fold-change (FC) were screened by gene chip, in which 171 genes showed up-regulated expression, and 176 genes showed down-regulated expression. The Bioinformation analysis results showed that these different genes distributed in several pathways, which were related to cancer, p53, MAPK, and interleukin-2 (IL-2) pathways and so on. Compared with control group, the relative expression levels of MAP2K, NR4A1, DUSP5, and DUSP6 mRNA in MAPK signaling pathway in WWOX over-expression group were increased (P<0. 05), and the relative expression level of fibroblast growth factor receptor 2 (FGFR2) mRNA was decresed (P<0. 05). Conclusion: The over-expression of WWOX gene in the Tca8113 cells can induce the changes of gene profile of Tca8113 cells. The tumor inhibition mechanism of WWOX gene may be related to regulating the expressions of some genes involving in MAPK signaling pathway.
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Objective The objective of this study was to investigate the inhibitory effect of MDM2 inhibitor Nultin-3 com-bined with cisplatin on human oral squamous cell carcinoma(OSCC)Tca8113 cells and its mechanism. Methods Human OSCC Tca8113 cells were treated with Nultin-3,cisplatin,Nultin-3 combined with cisplatin,or vehicle control groups. The proliferation of Tca8113 cells was determined by thiazolyl blue(MTT)assay. The expression of MDM2,P53,Caspase-9 and Caspase-3 protein was determined by Western blot. Results The proliferative rate of OSCC ca8133 cells treated with Nultin-3 combined with cisplatin was significantly lower than that of other groups(P<0. 05). The relative expression of Caspase-9,Caspase-3 and P53 protein in the Nultin-3 combined with cisplatin was significantly higher than those of the Nultin-3 and cisplatin alone groups(P<0. 05). In addi-tion,the relative expression of MDM2 protein in the Nultin-3 combined with cisplatin group was significantly lower than that of the cisplatin and Nultin-3 alone groups(P<0. 05). Conclusion Nultin-3 combined with cisplatin has synergistic effect on oral squa-mous cell carcinoma Tca8113 cells. Nultin-3 regulates the MDM2-p53 signaling pathway and up-regulates the expression of pro-apoptotic proteins Caspase-9 and Casapase-3 to enhance the inhibition of cisplatin on oral squamous cell carcinoma,providing a solid theoretical basis for clinical research and treatment.
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Objective:To investigate the effect of sorafenib on the proliferation of human oral cancer TCA8113 cells and to explore the underlying mechanisms.Methods:Mter treated with sorafenib at 2.5,5,10,20 μg/ml respectively for48 h,TCA8113 cell proliferation was examined by MTT and colony formation assay.Western blotting was employed to examine the p38MAPK expression in the cells.TCA8113 cells were pretreated with 10 μmol/L of SB203580 (a specific inhibitor of p38MAPK) for 30 min,and then by different concentrations of sorafenib for 48 h,cell proliferation was tested by MTT assay.Results:Sorafenib significantly inhibited the proliferation of TCA8113 cells in a concentration dependent fashion.Sorafenib also remarkably promoted the activation of p38MAPK of the cells.SB203580 significantly alleviated soiafenib induced TCA8113 cell viability decrease.Conclusion:Sorafenib can inhibit the proliferation of TCA8113 cells,which may be related to the activation of p38MAPK.
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Objective To observe the effect of curcumin combined with cisplatin on the proliferation of human tongue squamous cell carcinoma Tca?8113 cells,and explore the possible mechanism of their anti?tumor effect in vitro. Methods In this study,the samples were divided into four groups:curcumin,cisplatin,curcumin combined with cisplatin,and control. Detection of rate of inhibition of Tca?8113 cell proliferation was carried out by MTT assay. This was followed by observation of the morphological changes of the nuclei by Hoechst 33258 fluorescence staining. Subse?quently,cellular apoptosis was assayed by flow cytometry,and expression of Notch1 and epidermal growth factor receptor(EGFR)was examined by Western blotting. Results Results of MTT assay showed that curcumin combined with cisplatin inhibited the proliferation of tongue squamous cell carcinoma to a greater extent than either curcumin or cisplatin alone(P<0.05). Flow cytometry analysis indicated that,unlike curcumin or cisplatin alone,curcumin combined with cisplatin noticeably induced apoptosis(P<0.05). Results of Western blotting revealed that the expres?sion of Notch1 was upregulated,whereas the expression of EGFR was downregulated to a greater extent in the control group than in cells treated with curcumin or cisplatin alone. Unlike curcumin and cisplatin groups,the combined group revealed statistically significant expressions of Notch1 and EGFR(P<0.05). Conclusion Curcumin and cisplatin have a combined effect on inhibition of proliferation of human tongue squamous cell carcinoma Tca?8113 cells. The mechanism may be related to upregulation of the Notch1 signaling pathway and downregulation of the EGFR signal?ing pathway.
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Objective To compare the growth of three different cancer cell lines on chick chorioallantoic membrane (CAM), to select the best transplanted cancer cell line for establishing a transplanted tumor model and to observe the biological characteristics.Methods The human lung cancer cell line A549, human tongue cancer cell line TCA8113 and human liver cancer cell line QGY7703 were respectively inoculated into CAM at the 7th day of age.The chick embryo survival rate, tumor survival rate, tumor formation rate and induced angiogenesis were detected and the growth characteristics of the transplanted tumor model were observed.Results Compared with the groups inoculated with A549 cells and QGY7703 cells, the tumor formation rate of TCA8113 cells was the highest (P < 0.05), to be the best cancer cell line for transplanted tumor.The optimal inoculated number of cells was 8.0×106/chick embryo, the optimal growth period of the tumor was 4~8 d, and the best experiment time was 7 d after inoculation.Conclusion The TCA-CAM transplanted tumor model of tongue squamous cell cancer is successfully established for further study of the biological characteristics and mechanisms of tumor growth, angiogenesis, invasion and metastasis, and provide a good experimental animal model for anti-tumor drug screening.
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AIM:To investigate the effect of genistein on the proliferation of human oral cancer TCA 8113 cells and to explore the underlying mechanisms .METHODS:The cell proliferation was examined by MTT assay , cell counting and colony formation assay .Western blotting was employed to examine the protein levels of vascular endothelial growth fac -tor (VEGF), extracellular signal-regulated kinase (ERK) and p-ERK.RESULTS: Genistein significantly inhibited the proliferation of TCA8113 cells in a concentration-dependent fashion .Moreover , genistein dose-dependently decreased the protein levels of VEGF, ERK and p-ERK.The expression of VEGF was also blunted by U 0126, a specific inhibitor of ERK.U0126 and axitinib, a VEGF receptor antagonist , both significantly inhibited the proliferation of TCA 8113 cells. CONCLUSION:Genistein inhibits the proliferation of TCA8113 cells, which may be related to its inhibitory effect on ERK expression and activation , thus subsequently decreasing the expression of VEGF .
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Objective To investigate the possible mechanism of scutellarin on the apoptosis of human tongue squa?mous carcinoma Tca8113 cells. Methods Human tongue squamous carcinoma Tca8113 cells were divided into control group and scutellarin groups (80, 120 and 160 mg/L). Tunel method was used to detect the apoptosis. Immunohistochemistry and Western blot assay was used to detect the caspase-8 protein expression of cells. Results (1)The apoptotic rates of Tca8113 cells were significantly high in scutellarin groups (80, 120 and 160 mg/L) than those in control group [(17.63 ± 0.25)%, (36.23±0.36)%, (51.84±0.58)%vs (4.45±0.27)%, P<0.05].(2)Compared with control group, the expressions of cas?pase-8 protein were significantly increased in different concentrations (80, 120 and 160 mg/L) of scutellarin groups (0.283± 0.040 vs 0.474±0.031, 0.592±0.077, 0.781±0.020,P<0.05). Conclusion Scutellarin could obviously induce the apoptosis of human tongue squamous carcinoma Tca8113 cells, which may be related to the caspase-8 protein expression.
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Objective To explore the effect of proliferating cell nuclear antigen (PCNA) on apoptosis and proliferation of oral squamous cell carcinoma (OSCC) TCA8113 cells. Methods Hyper expressed plasmid pcDNA3.1-PCNA and RNA interference (RNAi) vector pSilencer-shPCNA were constructed and transfected into TCA8113 cells, and their expression was determined by Western blotting or Real-time PCR. The cell proliferation was then assessed using MTT assay. Cell apoptosis was detected by Annexin V/PI staining and flow cytometry, and the effects of PCNA hyper expression or gene silence on cell apoptosis were analyzed. Results PCNA hyper expression and down-regulation plasmid were constructed and transfected into TCA8113 cells successfully. The PCNA hyper expression and down-regulation were verified by Western blotting and Realtime PCR, respectively. MTT proliferation assay revealed that the PCNA hyper expression promoted TCA8113 cell proliferation. The survival rates of PCNA over-expressed cells at 24, 48 and 72h were significantly higher than those of control cells (P<0.05). PCNA silence effectively inhibited TCA8113 cell proliferation. The survival rates of PCNA down-regulated cells at 24, 48 and 72h were significantly lower than those of control cells (P<0.05). By treating with cisplatin, it was found that PCNA hyper expression inhibited cell apoptosis obviously, while PCNA silence facilitated cell apoptosis significantly. Conclusion PCNA gene is involved in the apoptosis and proliferation of OSCC TCA8113 cells, and it can significantly enhance the sensitivity of TCA8113 to chemotherapeutic drug cisplatin.
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Objective The purpose of this study was to investigate the effects of gossypol acetic acid (GAA) on protein and mRNA expressions of hMLH1 gene in human tongue carcinoma cell line Tca8113 in vitro in order to discuss the mechanism of tumor suppression of GAA. Methods (1) Western-blot was used to study the effects of GAA on protein expressions of hMLH1 gene in Tca8113 cell line treated by different concentrations of GAA for 48 h. (2) Real-time fluorescence quantitative PCR (RFQ-PCR) was used to investigate the effects on the mRNA expressions of hMLH1 gene in Tca8113 cell line treated by GAA for 48 h. Results (1) Compared with the control group, the results of Western-blot showed that the protein expression of hMLH1 gene was increased after treatment by GAA for 48 h ( <0.05) . (2) The results of RFQ-PCR indicated that the mRNA expression of hMLH1 gene was increased after GAA treatment for 48 h ( <0.05) . Conclusion GAA could up-regulate protein and mRNA expression of hMLH1 in Tca8113 cell line, which indicated that it may be one of the mechanisms of tumor suppression effect of GAA.
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Objective: To investigate the effects of GAA (gossypol acetic acid) on the proliferation, apoptosis and DNMT1 (DNA methyltransferase 1) mRNA expression of human tongue carcinoma cell line Tca8113 in vitro. Methods: The proliferation and apoptosis of Tca8113 cells after treatment with different concentrations of GAA were detected by MTT and flow cytometry, respectively. The expression level of DNMT1 mRNA was examined by real-time fluorescence quantitative-PCR. Results: The proliferative abilities of Tca8113 cells were inhibited after treatment with GAA for 24, 48, and 72 h. The apoptotic rates of Tca8113 cells after treatment with 30 μmol/L GAA for 48 h and 15 μmol/L GAA for 72 h were higher than those of the control cells (without GAA treatment) (P < 0.05). The expression levels of DNMT1 mRNA in Tca8113 cells after treatment with 5, 10, 15 and 20 μmol/L GAA for 48 h were lower than those of the control cells (P < 0.05). Conclusion: GAA can inhibit the proliferation and induce the apoptosis of human tongue carcinoma cell line Tca8113 with a decreased expression level of DNMT1 mRNA. Copyright © 2013 by TUMOR.
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Objective To investigate the mechanism of radiosensitization by cetuximab (C225) on human tongue cancer Tca8113 cell line in vitro.Methods Tca8113 cell line with and without C225 treatment received 6 MV X-ray irradiation of different doses (0, 2,4,6, 8 and 10 Gy). Cell proliferation,cell-cycle distribution and clonogenic survival were analyzed through cell counting,MTT,colony formation assay,and flow cytometry,respectively.Results After irradiation of different doses,the growth inhibition rates in C225 group were higher than control (t =- 15.6 - -3.0,P＜0.05),the radiobiological parameters (D0,Dq,N,and SF2 ) in C225 group were lower than control so that SER of C225 group was 1.353,and the proportions of G0/G1 cells in C225 group were higher than control ( t =-7.64,-7.89,-4.78,P ＜0.05 ) at 4,6,8 Gy.When the irradiation doses increased,the early phase apoptosis in both groups increased at first and then decreased with the maximum difference at 4 Gy [(7.96±0.36)％ in C225 group and (4.13 ±0.29)％ in control group,t =-12.75,P＜0.01 ].Conclusions C225 has radiosensitization effect on Tca8113 cell line,possible through Go/G1 arrest and induction of apoptosia.
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Aim To investigate the effects of sodium phenylbutyrate on cell proliferation,apoptosis and its expression of p21 and survivin genes in human tongue squamous cancer Tca8113 cell line.Methods The cellular proliferation inhibitory ratio was evaluated by MTT assay and the apoptosis and cell cycle of the Tca8113 cell line was detected by FCM.The expression of p21 and survivin genes was analyzed with Western blot and RT-PCR.Results Sodium phenylbutyrate could inhibit the Tca8113 cells proliferation,promote cell apoptosis and arrest the cells at G_1/G_0 phase.The expression of p21 gene in Tca8113 cell line treated by sodium phenylbutyrate was increased,and one of survivin gene was decreased.Conclusions Sodium phenylbutyrate induces up-regulation of p21 gene and down-regulation of survivin gene,which inhibits Tca8113 cell proliferation and induces its apoptosis and arrests the cells at G_1/G_0 phase.And the increase of p21 mRNA expression is negatively correlated with the decrease of survivin mRNA expression(r_s=-0.548,P<0.01),and so is its protein expression(r_s=-0.514,P<0.01).
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Objective: To investigate the effect of vitamin E succinate (VES) on apoptosis of Tca 8113 human oral squamous carcinoma cells and its action mechanism. Methods: Flow cytometry was applied to determine the effect of VES on cell cycle distribution and apoptosis after PI staining or Annexin V/PI double staining. The expression of Bax mRNA was quantified by RT-PCR. The relative amounts of the Bax protein was measured by Western blotting. Results: VES significantly inhibited the growth of Tca8113 cells, induced typical apoptosis, and up-regulated the expression of Bax mRNA and protein. After 24 h the apoptotic rate reached the peak level. Conclusion: VES induces apoptosis of Tca8113 human oral squamous carcinoma cells, which is probably related with up-regulation of Bax expression.
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To investigate the effects of ATRA, acitretin and tazarotene on the growth and apoptosis of human tongue squamous cell carcinoma cell line Tca8113. The effect of retinoids on growth of Tca8113 cells in vitro was examined by MTT assay and Trypan blue exclusion assay. Cell cycle analysis, early apoptosis analysis with double staining with Annexin V-FITC and PI, and active caspase-3 analysis with the staining of FITC-conjugated monoclonal rabbit anti-active caspase-3 antibody were made by flow cytometer. Streptavidin-biotin complex (SABC) immunocytochemical assays were employed for the detections of Bax/Bcl-2 proteins expressions. Our results showed that the retinoids inhibited growth of Tca8113 cells in a dose- and time-dependent manner with maximal inhibition 24 h after treatment of 10-5 mol/L. 10-5 mol/L retinoids altered cell cycle distribution of Tca8113 cells, revealing an increase in G0/G1-phase population, a decrease in S-phase population and the inhibition of G1/S switching. 10-5 mol/L retinoids significantly induced apoptosis of Tca8113 cells (all P<0.05), elevated the cells population with detectable active caspase-3 (P<0.05 for all), increased the number of cells forming Bax and decreased the number of cells forming Bcl-2 significantly (all P<0.05). Acitretin played a most prominent role among the retinoids. It is concluded that the inhibition of cell cycle progress of Tca8113 cells by ATRA, acitretin and tazarotene is one of the possible mechanisms for proliferation arrest of Tca8113 cells elicited by the retinoids. The retinoids mediate apoptosis in Tca8113 cells that may be caspase-dependent through mitochondria pathway. High concentration retinoids inhibit growth of Tca8113 cells in vitro by interfering with proliferation and inducing apoptosis of cells. Acitretin may be an alternative medicine for the prevention and treatment of tongue squamous cell carcinoma.
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Objective:To study the effects of hydroxycamptothecine(HC PT ) and pingyangmycin(PYM) alone or in combination(HCPT/PYM) on the proliferation and telomerase activity of human tongue carcinoma Tca 8113 cells.Methods :The growth inhibitary effects of HCPT or PYM on Tca 8113 cells were stu died by MTT assay and the IC 30 values of the two drugs were obtained. Then the cells were exposed to HCPT or PYM at IC 30 , or to their combination. T he clonogenecity, cell cycle distribution, morphological change and telomerase a ctivity were studied by clonogenic assay, flow cytometry,transmision electron mi croscopy and telomeric repeat amplification protocol (TRAP) respectively.Results:IC 30 (ng/ml) of HCPT and PYM was 109 and 416 respectivel y, when in combination(HCPT/PYM) the IC 30 of HCPT and PYM was 35 and 100 r espectively. The clonogenecity(%) of the control, HCPT,PYM and HCPT/PYM treated cells was 31.7,11.6,15.2 and 4.1 respectively. PYM decreased S and G 2 phase ce lls,increased G 1 phase cells.HCPT or HCPT/PYM decreased G 1 phase cells and i ncreased S and G 2 phase cells.Drug treatment resulted in cell organ degenerati on and decrese of telomerase activity.The A value at A 450 of telomerase in control,HCPT,PYM and HCPT/PYM treated cells was 1.89?0.03,0.82?0.02,0.77?0.0 2 and 0.53?0.02 respectively(P