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.
College of Chinese Medicine, North China University of Science and Technology, Tangshan 063000, China.
Yong-Sen
YS
Jia
Institute of Orthopaedics and Traumatology, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Xue-Qin
XQ
Hu
Health Science Department, Pecs University, Pecs 7622, Hungary.
Hegyi
H
Gabriella
School of Basic Medicine, North China University of Science and Technology, Tangshan 063000, China.
Li-Juan
LJ
Qin
First Department of Pathology & Experimental Cancer Research, Semmelweis University, Budapest 1085, Hungary.
Nora
N
Meggyeshazi