Background: FasL expression was reported to be associated with hepatic metastasis of colorectal cancer. The aim of this study was to study FasL gene expression in colorectal carcinoma and its influences on biological behavior and hepatic metastasis of colorectal carcinoma.
Methods: FasL gene expressions were examined with reverse transcriptase-polymerase chain reaction (RT-PCR) in the primary focus of colorectal carcinoma, adjacent cancerous mucosae, and metastasized liver focus from colorectal cancer. HR-8348 cells of human rectal cancer cell line were transfected with FasL cDNA. Cell growth suppression rate and response to 5-FU and carboplatin were observed and analyzed with the MTT method.
Results: FasL gene expression was detected in the primary focus of colorectal cancer (n=58), adjacent cancerous mucosae (n=58), and metastasized hepatic tumor tissues (n=28). The positive rate of FasL expression was 24% (14/58), 8% (5/58), and 100% (58/58) in the primary focus, adjacent cancerous mucosae and metastasized hepatic tumor tissues respectively. FasL expression rate in the metastasized hepatic tumor tissues was higher than that in the primary focus (X(2)=43.49, P<0.01) and adjacent cancerous mucosae (X(2)=57.66, P<0.01). In a group of patients with hepatic metastasis, the FasL expression rate in primary focus was higher than that in patients without hepatic metastasis (X(2)=3.96, P<0.05). In vitro study positive expression of FasL was shown in transfected HR-8348 cells. When 5-FU or carboplatin was added, there was a significant difference in growth suppression rate between FasL positive and controlled cancer cells (t=9.02, t=11.93, P<0.01). Under the same concentration of chemotherapeutic agents, the survival rate of FasL positive HR-8348 cells was higher than that of controlled cells.
Conclusions: FasL positive cancer cells are powerfully resistant to chemotherapeutic agents. The expression of the FasL gene in colorectal cancer cells is related to immune evasion to escape from being killed by immune cells, showing stronger drug-resistance, and it facilitates hepatic metastasis.