Journal of Experimental & Clinical Cancer Research 2008, 27:31 http://www.jeccr.com/content/27/1/31 Fas gene [22]. when studying the KLT- induced the apop- tosis of cancer cell(HL60), Li Y [19] make use of RT-PCR to detect the the gene expression of Fas, she observed that genetic transcription strengthened after 24 hours when using KLT at 10 ul/ml. Han SX [23] proved that KLT injec- tion can induce the apoptosis of human cervical carci- noma cell by raising the level of Fas gene. Similarly, the experiment, which detected the expression of Fas receptor on the surface of osteogenic sarcoma cell under different concentration of KLT [24], showed that under the KLT concentration of 0 ul/ml, 1 ul/ml, 5 ul/ml, 10 ul/ml and 20 ul/ml, the amount of Fas mRNA detected by the RT- PCR analisis is (0.12 ± 0.02) ul/ml, (0.27 ± 0.05) ul/ml, (0.35 ± 0.09) ul/ml, (0.46 ± 0.14) ul/ml and (0.51 ± 0.16) ul/ml respectively, so they considered that accompanied with the concentration of KLT increase, the level of Fas gene in the cancer cell significantly increased. Anyway, KLT may induce apoptosis of cancer cell by up-regulating the expression of Fas genes, but its effect on the Fas gene of liver cancer cell should be further studied. The effect of KLT on caspase-3 Caspases is a group of prolease that induce the apoptosis of cell. Under the normal circumstances, the strict sub- strate specificity and high effectivity of the activated cas- pases can assures its narrow spectrum of proteolysis during the process of apoptosis [25,26]. The caspases selectively Shear a group of protein in a simpatico way that lead to functional failure or structural changes of the protein. If the activity of caspases is suppressed, the cellu- lar apoptosis could be disturbed, which could lead to the occurrence and development of tumor, because the dynamic balance between cellular apoptosis and prolifer- ation is disturbed. Caspases-3 and Caspases-8 are the most widely studied in caspases family. Caspase-3, as a important member in the caspases family, is a major func- tional enzyme in the pathway of cellular apoptotic sig- nal[27,28]. Caspases-3 can cause the clearage of its substrate PARP(116 × 103) and transferred into opyeptide 24 × 103 and 89 × 103 and thereby activate the endonu- clease to trigger the complete degradation of DNA. Many factors that regulate the cellular apoptosis can react through caspase-3 prolease. The depressor of caspase-3 can restrain the activation of caspase-3 and degrade the activity of it, so that the apoptosis of cancer cell is restrained [29,30]. Bcl-2 and p53 both interact with cas- pase family [31-33]. Some report have discovered, while studying KLT-induced the apoptosis of human pancreatic cancer Paru-8988 cell, that the increase of caspase-3 total protein also show obviously time dependence [34]. More- over, through the test on the substrate of caspase-3-PARP, no degradation product (89 × 103) strap was found in the control group, but the degradation product (89 × 103) strap was discovered after 6 hours in KLT group, which indicates that caspase-3 have enzyme activity. However, no study or research about the effect of KLT on the liver cancer cell had done. The effect of KLT on other related genes PCNA (proliferating cell nuclear antigen) is a subunit of DNA polymerase and cell cycle-dependent protein whose maximum appearance in the S phase. Some research shows that the expression of PCNA is connection with the low grade tissues[35,36]. Wang JJ found that the gene expression of nuclear PCNA increased obviously, and the labeling index of PCNA was 15. 2% after 48 hours when 0.2 mg/ml KLT effected on the renal cancer cells, while hardly any gene expression of nuclear PCNA was observed in the control group [8]. They believed that PCNA took part in the reparative process of KLT- induced DNA injury, and when the degree of DNA injury is too serious to be repaired by PCNA, other genes such as P53 and Bcl-2 will send signals to trigger the apoptosis of cell and they were also convinced that the anticancer effect of KLT was a result of multiple gene interaction and restriction [8,15,16,19]. c-myc is one of the core protein – myc family in oncogene, and it not only is a positive controlling gene in cellular growth and cell life circle, but also take part in the progress of apoptosis, that is to say, it has dualism[37]. Under a cir- cumstances of growth inhibiting, improper expression of c-myc could induce regulatory failure of normal cell life circle and apoptosis[38]. when studying the KLT- induced the apoptosis of cancer cell(HL60), Li Y make use of RT- PCR to detect the the gene expression of c-myc, she observed that there was no significant change in genetic transcription after 24 hours when using KLT at 10 ul/ml [19]. As bcl-2 gene, we should do further research and study on it. P21WAFI/CIPI is the downstream gene of p53 gene, its acti- vation contain the p53 dependent path and the p53 non- dependent path[39]. The protein product of P21WAFI/CIPI can combine with cell circle protein, cyclin-dependent kinase(CDK), and proliferating cell nuclear anti- gen(PCNA) to form a quaternionic complex that can stop the cell life circle and depress the cell growth. Guo JW dis- covered that while up-regulate the expression of p53 pro- tein, KLT can raise the expression of p21WAFI/CIPImRNA and protein, it indicates that KLT can induce apoptosis of cancer cell by way of the p53 dependent path to up-regu- late the expression of p21WAFI/CIPI [16]. Furthermore, some researchers found that KLT can up-reg- ulate the level of ubiquitin C, RAD17 genes and down reg- ulate t the level of cyclin A, cyclin E1, cyclin F gene in studying the influence of KLT on Patu-8988 cell life circle and gene expression [40]. Page 3 of 5 (page number not for citation purposes)