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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- κ B 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- κ B 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- κ B 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- κ B 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- κ B transduction cascade.

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