Journal of Experimental & Clinical Cancer Research 2008, 27:31 http://www.jeccr.com/content/27/1/31 In addition, some study [41] show that the genes regu- lated apoptosis are not isolated, they can influence and restrict with each other, for example, Bcl-2 family, IAPs family, c-myc, P53, P35, can affect activation of caspase-3 through regulating activation of caspase-8 and caspase- 9[42]. so Kanglaite may promote the interaction of those genes to form a network cycle, amplify cascade reaction and further promote apoptosis. but there is no related research at the present stage. Conclusion Now, the study of KLT-induced apoptosis is focused on the above-mentioned gene. In short, KLT induce apopto- sis of cancer cell by way of up regulating the expression of p53 gene, Fas gene, Caspase-3, PCNA, p21WAFI/CIPI and down regulating the expression of cyclin A, cyclin E1, cyc- lin F gene. But its effect on the expression of bcl-2 gene and c-myc gene is not yet clear. The occurrence of malignant tumor may be caused by the abnormal proliferation of cell or the inhibition of cellular apoptosis pathway. The proliferation of tumor cell and the apoptosis of tumor cell are not only affected by many factors and pathways such as drugs, radioactive ray, etc, but also regulated by some tumor genes or tumor-sup- pressing gene. It has been proved that the Chinese crude drug-induced apoptosis is one important anticancer mechanism of Chinese crude drug, and it is also relevant to the concentration of the medicine[43]. Just as the result of experimental treatment on hepatoma of mice that we have done [44], we found that KLT can made the cancer cells stop in the G2+M phase of cell life circle, and prevent them form entering the G0 and G1 phase. so it can induce the apoptosis and suppress growth of cells without any effect on the surrounding normal tissues or causing Inflammatory reaction which are unique characteristics. based on these characteristics, KLT has been used in the treatment on many kinds of malignant tumor, and the clinical effect show that KLT can not only repress tumor directly, improve the quality of life obviously, enhance the patient's immunity, but also enhance the effectiveness of chemotherapy and reduce side effects [45-47], which is consistent with its pharmacology above-mentioned How- ever, the relationship between the apoptosis of hepatoma carcinoma cell and gene is further studied, although these research can not fully reveal the mechanism of KLT- induced apoptosis, and its experimental result is still pre- liminary, the trend of using KLT to prevent and cure liver cancer is already formed, and with the development of modern medical technologies, its mechanism will undoubtedly be revealed in the near future. and KLT will bring new hope for the treatment of cancer and the pro- tection of normal tissues with the more sufficient evi- dence of its effect on liver cancer and other tumor in clinical trials. Competing interests The authors declare that they have no competing interests. Authors' contributions LY wrote the article under the supervision of DQ. LY, LCS and DQ contributed to the collection and evaluation of date. LY conceived of the study, and participated in its design and coordination. All authors read and approved the final manuscript. References 1. Liang J, Luo G, Ning X, Shi Y, Zhai H, Sun S, Jin H, Liu Z, Zhang F, Lu Y, Zhao Y, Chen X, Zhang H, Guo X, Wu K, Fan D: Differential expression of calcium-related genes in gastric cancer cells transfected with cellular prion protein. Biochem Cell Biol 2007, 85:375-383. 2. Tschaharganeh D, Ehemann V, Nussbaum T, Schirmacher P, Breuhahn K: Non-specific effects of siRNAs on tumor cells with impli- cations on therapeutic applicability using RNA interference. Pathol Oncol Res 2007, 13:84-90. 3. Chase A, Grand FH, Cross NC: Activity of TKI258 against pri- mary cells and cell lines with FGFR1 fusion genes associated with the 8p11 myeloproliferative syndrome. Blood 2007, 110:3729-3734. 4. Ghosh AK, Varga J: The transcriptional coactivator and acetyl- transferase p300 in fibroblast biology and fibrosis. J Cell Physiol 2007, 213:663-671. 5. Li DP: Progress on mechanism of KLT injection antitumous effect. Traditional Chinese Drug Research & Clinical pharmacology 2001, 2:122-124. 6. Wei CY, Tang ZP, Tang K: The experimental study on cytotox- icity of primary liver cancer which caused by extract of coix- enolide. Journal of Cancer Prevention & Treatment 2000, 7:610-611. 7. Feng B, Liu JH: The alleviative KLT Injection treatment on malignant tumor in advanced stage. Chinese Journal of Clinical Oncology 1999, 26:238-240. 8. Wang JJ, Sun XC, Shen WJ: Research on apoptosis of cancer cell and expression of p53, bcl-2 protein Induced by KLT Injec- tion. Chinese Journal of Clinical Oncology 1999, 26:439-442. 9. Ma L, Wen S, Zhan Y, He Y, Liu Y, Jiang J: Anticancer effects of the Chinese medicine matrine on murine hepatocellular carci- noma cells. Planta Med 2008, 74:245-251. 10. Qian J, Feng GS, Vogl T: Combined interventional therapies of hepatocellular carcinoma. World J Gastroenterol 2003, 9:1885-1891. 11. Werkgartner G: Portal vein embolization before major hepa- tectomy and its effects on regeneration, resectability and outcome (Br J Surg 2007; 94: 1386–1394). Br J Surg 2008, 95:398-399. 12. Wei CY, Li T, Tang ZP: Study of coicis seed extract in its effec- tion inducing proliferation, apoptosis and expression of p53 in human hepatocellular carcinoma. Journal of Guangxi Medical University 2001, 18:793-795. 13. Tanigawa S, Fujii M, Hou DX: Stabilization of p53 is involved in quercetin-induced cell cycle arrest and apoptosis in HepG2 cells. Biosci Biotechnol Biochem 2008, 72:797-804. 14. Casavant NC, Luo MH, Rosenke K, Winegardner T, Zurawska A, For- tunato EA: Potential role for p53 in the permissive life cycle of human cytomegalovirus. J Virol 2006, 80:8390-8401. 15. Bao Y, Xia L, Jiang H: The experiment and study on cellular apoptosis Induced by KLT injection in pancreatic cancer cell. Shanghai Journal of Medicine 2004, 27:421-424. 16. Guo JW, Shen ZZ, Luo JM: Study on apoptosis and cell cycle arrest Induced by Kanglaite in multidrug resistant human breast cancer cell line MCF7. Chinese Journal of Integrative Medi- cine 2001, 6:123-125. 17. Kuntzen C, Zazzeroni F, Pham CG, Papa S, Bubici C, Knabb JR, Fran- zoso G: A method for isolating prosurvival targets of NF-kap- paB/Rel transcription factors. Methods Mol Biol 2007, 399:99-124. 18. Hall JL: Discovery of an intricate balance. Gene transcription, cell cycle, and apoptosis. Circ Res 2008, 102:395-397. Page 4 of 5 (page number not for citation purposes)