Overexpression of Stimulates Paclitaxel to Inhibit Malignant Behaviors of Hepatocellular Carcinoma Cells.

OBJECTIVE

Explore the effect of expression on Paclitaxel inhibiting growth of hepatocellular carcinoma (HCC) cells.

MATERIALS AND METHODS

In the experimental study, HCC cell lines (HLE, Bel7402 and PLC/PRF/5) were treated with different concentrations of Paclitaxel (5-20 mg/ml) for 24 hours. HLE cells were transfected with -siRNA vector, while Bel7402 and PLC/PRF/5 cells were transfected with overexpressed GATA5 vector for 24 hours, followed by treatment of the cells with Paclitaxel (10 mg/ml) for 24 hours and subsequently 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay to detect growth of HCC cells. Soft agar cultured was used to analyze formation of colony. Apoptosis of HCC cells were detected by Flow cytometer. Migration of HCC cells was observed by trawell assays. Western blotting and laser confocal microscopy were utilized to detect expression and location of the proteins.

RESULTS

Inhibiting expression of reduced sensitivity of HLE cells to Paclitaxel, while overexpression of increased sensitivity of Bel7402 cells and PLC/PRF/5 cells to Paclitaxel. Overexpression of played a role in stimulating Paclitaxel to inhibit growth, colony formation and migration, as well as enhance apoptosis in HCC cells. Overexpression of also promoted Paclitaxel to inhibit expression of reprogramming genes, such as Nanog, and in Bel7402 and PLC/PRF/5 cells. Inhibited expression of led to enhancement of the expression of CD44 and CD133, in HLE cells. Overexpression of was not only alone but also synergized with Paclitaxel to inhibit expression of CD44 and CD133 in Bel7402 or PLC/PRF/5 cells.

CONCLUSION

Overexpression of played a role in enhancing Paclitaxel to inhibit the malignant behaviors of HCC cells. It was involved in suppressing expression of the reprogramming genes and stemness markers. Targeting is an available strategy for applying paclitaxel to therapy of patients with HCC.