Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways

Background:Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis.However,whether it also has anticancer activities in KOSC3 cells,an oral cancer cell line,is unclear.Methods:3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide,flow cytometry,and western blotting assays were carried out to assess cell viability,subG1 phase of the cell cycle,and apoptosis-related protein expression,respectively.Results:Ourfindings indicate that paclitaxel could inhibit cell viability and increase the expression of apoptotic markers,including plasma membrane blebbing and the cleavage of poly ADP-ribose polymerase in KOSC3 cells.Also,the treatment with paclitaxel remarkably elevated the percentage of the subG1 phase in KOSC3 cells.In addition,treatment with a pan-caspase inhibitor could recover paclitaxel-inhibited cell viability.Moreover,caspase-8,caspase-9,caspase-7,and BH3 interacting domain death agonist(Bid)were activated in paclitaxel-treated KOSC3 cells.Conclusions:Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells.

miR-106b promotes cancer progression in hepatitis B virusassociated hepatocellular carcinoma

AIM: To investigate the effect of mi R-106 b on tumor progression in hepatitis B virus(HBV)-associated hepatocellular carcinoma(HCC).METHODS: A total of 120 patients who underwent liver resection for HCC at National Cheng Kung University Hospital were enrolled in the present study. Micro RNA(mi RNA) array was first used to screen the mi RNA expression profiles in HCC patients. The clinical records were retrospectively analyzed, and correlations with the mi RNA expression profiles were evaluated. The m RNA expression levels of the mi R-106b-25 cluster(mi R-106 b, mi R-93 and mi R-25), and MCM7 in tumor and non-tumor samples were quantitated using quantitative real-time reverse transcription-polymerase chain reaction(q-RT-PCR) analysis, and correlations in the levels of mi R-106 b, mi R-93 and mi R-25 expression were calculated. Kaplan-Meier overall and diseasefree survival rates of HBV-associated HCC patients were analyzed using the log-rank test based on mi R-106 b expression. The comparison of the mi R-106 b expression levels in patients with different clinical outcomes was analyzed using Mann-Whitney U tests. Furthermore, a hepatitis B virus X protein(HBx) expression plasmid was transfected into Huh7 and Hep 3B cells. The expression levels of the mi R-106b-25 cluster and MCM7 in HBx-expressing Huh7 and Hep 3B cells were detected using q-RT-PCR. RESULTS: mi RNA array screening showed that mi R-106 b and its cluster, mi R-93 and mi R-25 were upregulated in HCC patients(P < 0.01). The value of mi R-106 b expression in HBV-associated HCC patients was significantly higher than that in HCV-(P < 0.05) or non-B/non-C-(P < 0.001) associated HCC patients. The expression of the mi R-106b-25 cluster was significantly higher in tumor tissue(P < 0.001) and associated with the host gene, MCM7, in clinical specimens from HBVassociated HCC patients. Furthermore, the expression levels of mi R-106 b, mi R-93 and mi R-25 were positively correlated in HBV-associated HCC tissues(mi R-106 vs mi R-93, r = 0.75; mi R-93 vs mi R-25, r = 0.69; mi R-106 b vs mi R-25, r = 0.33). The overall and diseasefree survival curves showed that high-mi R-106 b expression was correlated with the poor prognosis of HBV-associated HCC. HCC differentiation was significantly correlated with mi R-106 b expression(P < 0.05). Lower mi R-106 b expression levels resulted in the well differentiation of HCC. Moreover, the expression of the mi R106b-25 cluster and MCM7 was up-regulated in Huh7 and Hep 3B cells after transfection with the HBx expression plasmid.CONCLUSION: The data obtained in the present study suggests that HBx enhances mi R-106 b transcription to promote tumor progression in HBV-associated HCC.