Proliferation Inhibitory Activity of Quinones from Blaps rynchopetera Defense Secretion on Colorectal Tumor Cells

Objective: To explore the proliferation inhibitory effect of quinones from Blaps rynchopetera defense secretion on colorectal tumor cell lines. Methods: Human colorectal cancer cell HT-29, human colorectal adenocarcinoma cell Caco-2 and normal human colon epithelial cell CCD841 were chosen for the evaluation of inhibitory activity of the main quinones of B. rynchopetera defense secretion, including methyl p-benzoquinone (MBQ), ethyl p-benzoquinone (EBQ), and methyl hydroquinone (MHQ), through methyl thiazolyl tetrazolium assay. The tumor-related factors, cell cycles, related gene expressions and protein levels were detected by enzyme-linked immunosorbent assy, flow cytometry, RT-polymerase chain reaction and Western blot, respectively. Results: MBQ, EBQ, and MHQ could signifificantly inhibit the proliferation of Caco-2, with half maximal inhibitory concentration (IC50) values of 7.04 +/- 0.88, 10.92 +/- 0.32, 9.35 +/- 0.83, HT-29, with IC50 values of 14.90 +/- 2.71, 20.50 +/- 6.37, 13.90 +/- 1.30, and CCD841, with IC50 values of 11.40 +/- 0.68, 7.02 +/- 0.44 and 7.83 +/- 0.05 mu g/mL, respectively. Tested quinones can reduce the expression of tumor-related factors tumor necrosis factor a, interleukin (IL)-10, and IL-6 in HT-29 cells, selectively promote apoptosis, and regulate the cell cycle which can reduce the proportion of cells in the G1 phase and increase the proportion of the S phase. Meanwhile, tested quinones could up-regulate mRNA and protein expression of GSK-3 beta and APC, while down-regulate that of beta-catenin, Frizzled1, c-Myc, and CyclinD1 in the Wnt/beta-catenin pathway of HT-29 cells. Conclusion: Quinones from B. rynchopetera defense secretion could inhibit the proliferation of colorectal tumor cells and reduce the expression of related factors, which would be functioned by regulating cell cycle, selectively promoting apoptosis, and affecting Wnt/beta-catenin pathway-related mRNA and protein expressions.