Anti-tumor effect of Huayu Jiedu formula on SGC-7901 cancer cell
DOI:
https://doi.org/10.3329/bjp.v11i0.26689Keywords:
Anti-tumor, Huayu Jiedu, SGC-7901 cancer cellAbstract
In this study, we evaluated the effects of the extract of Huayu Jiedu (HYJD) formula on anti-tumor activity. It was found that HYJD treatment inhibited proliferation of seven cancer cell lines (IC50: 1.23-6.23 mg/mL). The gastric cancer cell line SGC-7901 was the most sensitive to HYJD. HYJD inhibited SGC-7901 cells proliferation in a dose- and time-dependant manner. More-over, HYJD significantly inhibited SGC-7901 cells adhesion, invasion and migration in a dose-dependent manner. qPCR results showed that HYJD treatment had no effect on PI3K, PDK1 and Akt mRNA expression. However, HYJD dramatically down-regulated Akt phosphorylation through inhibition of PDK1 kinase activity. Importantly, HYJD inhibited growth of tumor xenografts with no effect on body weight and spleen index. HYJD also significantly down-regulated Akt phosphorylation in tumor tissue. Taken together, this study demonstrated that HYJD exhibited an anti-tumor property, suggesting that HYJD may be a potential drug in the treatment of cancer.
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References
Belham C, Wu S, Avruch J. Intracellular signalling: PDK1-a kinase at the hub of things. Curr Biol. 1999; 9: R93-96.
Cao Y, Xia QH, Meng H, Zhong AP. Anti-tumor and synergistic effect of Chinese medicine "bushen huayu jiedu recipe" and chemotherapy on transplanted animal hepatocarcinoma. World J Gastroenterol. 2005; 11: 5218-20.
Cao Y, Xia QH, Meng H, Zhong AP. Pharmacological effects of serum containing Chinese medicine Bushen Huayu Jiedu compound recipe in lung cancer drug-resistance cells. Chinese J Integr Med. 2008; 14: 46-50.
Efferth T, Li PC, Konkimalla VS, Kaina B. From traditional Chinese medicine to rational cancer therapy. Trends Mol Med. 2007; 13: 353-61.
Engelman JA. Targeting PI3K signalling in cancer: Opportunities, challenges and limitations. Nat Rev Cancer. 2009; 9: 550-62.
Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000; 100: 57-70.
Hidalgo M, Rowinsky EK. The rapamycin-sensitive signal transduction pathway as a target for cancer therapy. Oncogene 2000; 19: 6680-86.
Hood JD, Cheresh DA. Role of integrins in cell invasion and migration. Nat Rev Cancer. 2002; 2: 91-100.
Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011; 61: 69-90.
Jiang WY. Therapeutic wisdom in Traditional Chinese Medicine: A perspective from modern science. Discovery Med. 2005; 5: 455-61.
Li X, Yang G, Li X, Zhang Y, Yang J, Chang J, Sun X, Zhou X, Guo Y, Xu Y, Liu J, Bensoussan A. Traditional Chinese Medicine in cancer care: A review of controlled clinical studies published in Chinese. PLoS One 2013; 8: e60338.
Sampedro Camarena F, Cano Serral G, Sampedro Santalo F. Telomerase and telomere dynamics in ageing and cancer: Current status and future directions. Clinical and translational oncology: Official publication of the Federation Spanish Oncology Societies and of the National Cancer Institute of Mexico. 2007; 9: 145-54.
Schmidt M, Hovelmann S, Beckers TL. A novel form of constitutively active farnesylated Akt1 prevents mammary epithelial cells from anoikis and suppresses chemotherapy-induced apoptosis. Bri J Cancer. 2002; 87: 924-32.
Serra V, Markman B, Scaltriti M, Eichhorn PJ, Valero V, Guzman M, Botero ML, Llonch E, Atzori F, Di Cosimo S, Maira M, Garcia-Echeverria C, Parra JL, Arribas J, Baselga J. NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations. Cancer Res. 2008; 68: 8022-30.
Shen X, Xi G, Radhakrishnan Y, Clemmons DR. PDK1 recruit-ment to the SHPS-1 signaling complex enhances insulin-like growth factor-i-stimulated AKT activation and vascular smooth muscle cell survival. J Biol Chem. 2010; 285: 29416-24.
Siegel R, Ma J, Zou Z, Jemal A. Cancer statistics, 2014. CA Cancer J Clin. 2014; 64: 9-29.
Toker A, Newton AC. Cellular signaling: Pivoting around PDK-1. Cell 2000; 103: 185-88.
Wang L, Zhou X, Zhou T, Ma D, Chen S, Zhi X, Yin L, Shao Z, Ou Z, Zhou P. Ecto-5'-nucleotidase promotes invasion, migration and adhesion of human breast cancer cells. J Cancer Res Clin Oncol. 2008; 134: 365-72.
Zhang F, Jia Z, Deng Z, Wei Y, Zheng R, Yu L. In vitro modulation of telomerase activity, telomere length and cell cycle in MKN45 cells by verbascoside. Planta Medica. 2002; 68: 115-18.
Zhang L, Zhang J, Chen J, Xing D, Mu W, Wang J, Shang H. Clinical research of Traditional Chinese Medicine needs to develop its own system of core outcome sets. Evid Based Complement Alternat Med. 2013; 2013.
Zimmermann S, Martens UM. Telomeres and telomerase as targets for cancer therapy. Cell Mol Life Sci. 2007; 64: 906-21.
Additional Files
- sound
- Figure 1: HPLC analysis of extract of HYJD and chemical profile
- Figure 2: HYJD inhibited proliferation of various cancer cell lines
- Figure 3: HYJD significantly inhibited adhesive, migratoryand invasive abilities of SGC-7901 cells
- Figure 4 : HYJD down-regulated phosphorylation of Akt protein in SGC-7901 cells
- Figure 5: HYJD dramatically suppressed PDK1 kinase activity in vitro
- Figure 6: HYJD inhibited the growth of tumor xenografts in vivo
- Figure 7: The effects of HYJD on body weight and spleen index
- Figure 8: HYJD down-regulated phosphorylation of Akt protein in tumor tissue
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