[Effect of Brucea Javanica Oil Emulsion on the Invasiveness of Glioma Cells and Its Possible Mechanism].

OBJECTIVE: To investigate the effect of brucea javanica oil emulsion on the invasiveness of glioma cells and hosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) signaling pathway. METHODS: C6 glioma cells were treated by brucea javanica oil emulsion. The inhibition rate of glioma cells was detected by MTT, Western blot was used to detect protein expression levels of PI3K, AKT, and nuclear factor (NF)-κB in glioma cells. The number of the glioma cells migrated through polycarbonate membrane was detected by crystal violet staining method. RESULTS: Brucea javanica oil emulsion inhibited PI3K, AKT, and NF-κB protein expression which reached the highest inhibition at 30 min, 60 min, and 120 min after brucea javanica oil emulsion, respectively. Maximum suppression on the proliferation of C6 glioma cells reached at 180 min after brucea javanica oil emulsion, while the number of glioma cells migrated through polycarbonate membrane was the least. CONCLUSION: Brucea javanica oil emulsion inhibit the proliferation and invasiveness of glioma cells, which may be related to the inhibition of PI3K/AKT signal pathway.

Tonglian Decoction () arrests the cell cycle in S-phase by targeting the nuclear factor-kappa B signal pathway in esophageal carcinoma Eca109 cells.

OBJECTIVE: To investigate the anti-tumor activity and molecular mechanism of Tonglian Decoction (, TLD) on esophageal carcinoma Eca109 cells. METHODS: Eca109 cells were treated with TLD and its separated formulae, including the clearing-heat and detoxification formula (Q), activating-blood and promoting-qi formula (H) and nourishing-yin and blood formula (Z). Cell proliferation was measured using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, cell morphology was observed using a microscope, the cell cycle was measured using flow cytometry and the activity of the nuclear factor-kappa B (NF-κB) signal pathway was detected by Western blot. RESULTS: The half maximal inhibitory concentrations of TLD, Q and H were 386, 771 and 729 mg/L, respectively. TLD, Q and H significantly inhibited cell proliferation, with 69.43%, 60.84% and 61.90% of treated cells in the G phase of the cell cycle. The percentage of cells in S phase increased significantly after treatment with TLD, Q, and H compared with the control group (P<0.05), and TLD showed the strongest effect. Z had no influence on the cell cycle compared with the control group (P>0.05). Western blot detection indicated slight differences in the inhibition of the NF-κB pathway by the different formulae. TLD formula strongly inhibited IKKß, NF-κB, interleukin-6 and tumor necrosis factor-α expression compared with the control group. CONCLUSIONS: TLD inhibited Eca109 cell proliferation by arresting cells in S phase. The possible mechanism might be related to inhibiting the NF-κB transduction cascade. The combination of the herbs found in the three separate formulae, H, Q and Z, work synergistically in TLD to produce the inhibitory effects of TLD treatment on Eca109 proliferation.

Antitumor Activity of Tenacissoside H on Esophageal Cancer through Arresting Cell Cycle and Regulating PI3K/Akt-NF-κB Transduction Cascade.

Objective. The purpose of the study was to elucidate the molecular mechanism of tenacissoside H (TDH) inhibiting esophageal carcinoma infiltration and proliferation. Methods. In vitro, EC9706 cells were treated with TDH. Cells proliferation and cell cycle were assayed. PI3K and NF-κB mRNAs expression were determined by real time PCR. In vivo, model of nude mice with tumor was established. Mice were treated with TDH. Inhibition ratio of tumor volume was calculated. PCNA expression was examined. Protein expression in PI3K/Akt-NF-κB signaling pathway was determined. Results. In vitro, TDH significantly inhibited cells proliferation in a time-and-dose-dependent manner. TDH arrested the cell cycle in S phase and significantly inhibited PI3K and NF-κB mRNA expression, compared with blank controlled group (P < 0.05). In vivo, TDH strongly inhibits tumor growth and volume. PCNA expression was significantly decreased after treatment of TDH. TDH downregulated proteins expression in PI3K/Akt-NF-κB transduction cascade (P < 0.05). Conclusion. TDH inhibited esophageal carcinoma infiltration and proliferation both in vitro and in vivo. The anticancer activity has relation to arresting the cell cycle at the S phase, inhibited the PCNA expression of transplanted tumors in nude mice, and regulated the protein expression in the PI3K/Akt-NF-κB transduction cascade.