The Vitro Research Of The Effect Of Beclin1on Paclitaxel-sensitivity In Laryngeal Carcinoma Cell Hep-2

BackgroundLaryngeal squamous cell carcinoma (LSCC) is one of the most common malignant tumor of head and neck region in the world. At present, surgery combined with radiotherapy and chemotherapy is the primary therapy of LSCC.Chemotherapy resistance limits its effects. Autophagic cell death is Ⅱ type of programmed cell death, it is different from apoptosis and caspase-independent. Beclinl is a critical mammalian autophagy gene. Beclin1can stimulate autophagy and involves an interaction with apoptotic pathway. The roles and mechanisms of Beclinl in human laryngeal squamous cell carcinoma progression has not yet been fully characterized. So we detect the effects of Beclinl on paclitaxel-sensitivity in laryngeal carcinoma cell.MethodsThis study used Hep-2, Hep-2-pcDNA3.1, Hep-2-Beclinl as vitro model. The effect of paclitaxel on the proliferation and cell apoptosis of laryngeal cancer cell lines was evaluated by MTT assay and flow cytometry. The protein expression level of Akt and p-Akt was detected by western blot.Results After treated by paclitaxel, the inhibition rate was significantly higher in Hep-2-Beclin cells than in Hep-2-pcDNA3.1cells and Hep-2cells (P<0.05). After dealing with10μg/L paclitaxel, the apoptosis rate in Hep-2, Hep-2-pcDNA3.1,Hep-2-Beclinl were23.75%±3.77%,21.25%±4.92%,32.50%±5.97%, respectively. After dealing with20μg/L paclitaxel, the apoptosis rate in Hep-2, Hep-2-pcDNA3.1, Hep-2-Beclin1were38.75%±4.79%,38.75%±6.55%,50.00%±7.26%, respectively. Paclitaxel-induced apoptosis was higher in Hep-2-Beclin cells than in Hep-2-pcDNA3.1cells and Hep-2cells (P<0.05). The result of western blot showed that the protein expression level of p-Akt in Hep-2-Beclin cells was lower than in Hep-2-pcDNA3.1cells and Hep-2cells (P<0.05) and the protein expression level of Akt was similar in three cell lines (P>0.05).ConclusionsBeclinl enhances paclitaxel-sensitivity by inhibition of PI3K/Akt pathway.