Journal of Experimental & Clinical Cancer Research 2008, 27:31 http://www.jeccr.com/content/27/1/31 of cells, so the proliferation of tumor cell was inhibited, at the same time it can also activate some pro-apoptotic fac- tor, and further lead to apoptosis [8]. Clinical application also shows that combined with chemotherapy, KLT has a good effect on the treatment of advanced cancer, particu- larly in digestive tract cancer, for example, the patient's life span and quality of life improve significantly. The finding show that this preparation has significantly depressant effect and preonunced curative effect on a variety of cancer cells [9]. Although the therapeutic measure of liver cancer contain surgery, radiotherapy, chemotherapy, interven- tional therapy and so on, their effect is not satisfactory so far [10,11]. However, with the development of cell biol- ogy, the theory of apoptosis presents a new hope and path for the treatment of liver cancer, The present study has found that KLT plays an important role in promoting apoptosis of hepatoma cells [12]. It has been known that the apoptosis of hepatoma cells is triggered by a variety of receptor-mediated cell signaling, and a variety of protease take part in the apoptotic signal transduction. In addition many kinds of genes are also involved with apoptotic reg- ulation of hepatoma cells. In this paper, the relationship between KLT and the hepatoma cell apoptosis molecules is going to be discussed and reviewed generally. The influence of KLT on p53 There are two types of p53 genes: the wild type p53 gene and the mutant p53 gene. The wild type p53 gene, which is also known as the guardian of gene, is indispensable to regulate the normal cells circle [13,14]. On the one hand, as the important regulating factor in the process of apop- tosis, the wild type p53 monitor the integrity of genes all the time, on the other hand, as the nuclear transcripton, it can respectively combines with DNA and RNA polymer- ase to regulate expression of gene, it can also inhibit the synthesis of DNA, take part in the repair of DNA, induce cell growth stop at the phase of G0. In addition, the wild type p53 gene can induce the Fas-mediated cell proce- dural death after the damage of DNA, so that the regular growth of cell is maintained. Wang JJ [8] had found, while discussing the anticancer mechanism of KLT injection, that the labeling index of wild type p53 in treat group which received KLT injection is 16.8%, while the control group had no expression at all. Furthermore, in the exper- iment about KLT-induced apoptosis, Bao Y [15] discov- ered that compared with the control group, the mRNA level of the wild type p53 gene significantly Increased in 20 μl/ml KLT experimental group after 48 hours. And in the experiment about apoptosis of multidrug resistance phenotypic human breast cancer cell line MCF7adr and its cell cycle arrest that induced by KLT. According to the immunohistochemical detection, Guo JW [16] found that the wild type p53 gene of MCF7adr in the control group is negative, but the wild type p53 gene of MCF7adr in the KLT experimental group is midrange positive, it can be assumed that KLT could up-regulate the expression of p53 and extend half life of p53 protein. In addition, Wei CY [12] observed 34 cases' hepatoma carcinoma cell that cul- tivated in vitro and their changes after treated with KLT, the results indicated that, compared with the control group, the apoptosis of hepatoma carcinoma cell in KLT experimental group is very significant, there was signifi- cant difference between them, at the same time, the labe- ling index of wild type p53 in the treat group is (8.39 ± 1.42)%, but the labeling index of wild type p53 in the control group (2.11 ± 0.97)%, there was significant differ- ence between these two groups. the phenomenon recorded here is the same as the studies of Wang JJ, Guo JW and Bao Y which had indicated [8,15,16]. In conclu- sion, KLT injection's may induce the apoptosis of tumor cell by way of up-regulate the expression of p53 genes. The effect of KLT on the bcl-2 genes Proto-oncogenes bcl-2 is the most definite apoptotic antagonist gene so far. In 1984, It was first cloned in t(14; 18) (q32; q21) chromosome translocation of follicular lymphoma cell line. But many studies had also confirmed that the high expression of this gene might inhibit the apoptosis of a variety of cells as well[17,18], thereby it can participate in the occurrence of a variety of tumor. When studying the anticancer mechanism of KLT, Wang JJ [8] found that the labeling index of bcl-2 gene was (16.80 ± 3.77)% in the control group, which is higher than that (6.6%) in the 10 μl/ml KLT treat group. Moreover, accom- panied with the concentration of KLT increase, the gene expression of bcl-2 decreased in KLT group. In the experi- ment about KLT-induced the apoptosis of pancreatic can- cer cells, according to the Western blot analysis, Bao Y [15] discovered that the expression of bcl-2 protein decreased after 72 hours when application of KLT at 20 μl/ml, the results of these two experiments above-mentioned may indicate that KLT induced the apoptosis of cells by down- regulating the expression of bcl-2 genes. Nevertheless, when studying the KLT- induced the apoptosis of cancer cell(HL60), Li Y [19] make use of RT-PCR to detect the the gene expression of bcl-2, there was no significant change in genetic transcription after 24 hours when using KLT at 10 ul/ml. So, whether KLT induces apoptosis of cancer cell by down-regulating the expression of bcl-2 genes isn't yet clear, and its role in hepatoma is not learned, which requires further study and research. The effect of KLT on Fas-genes Fas gene is located on the No.10 chromosome q23, with a length about 25 kb, the codogenic Fas protein consists of 325 amino acids and it can be expressed in many tis- sues. When Fas protein combining with Fas ligand, signal of apoptosis is send to the cell and the apoptosis of cell is induce [20,21] Many anticancer drugs can induce the apoptosis of cancer cell by up-regulating the expression of Page 2 of 5 (page number not for citation purposes)