Abstract: ObjectiveTo observe the effect of Galectin-3 gene knock out to the mouse skin tumor growth and discuss the mechanism of inhibition of the mouse cutaneous tumor induced by TPA which caused by Galectin-3 knock out. MethodsThe DMBA + TPA multi-step induced skin tumor in mice model were used to establish the skin cancer model. The control group was the same age wild type mice. We observed the inhibition of the mouse tumor growth by Galectin-3 knock out. In situ tumor cells were collected and cultured on soft agar for colony formation assay. The side population of the situ cancer cells was analyzed quantitatively by flow cytometry. Results1. Compared with wild type mice group (group A), Galectin-3 knock out mice group (group B) displayed a significant delay of the appearance of tumor. The tumor incidence and the average number of tumor per mice between group A and group B had obvious difference (P < 0.01). 2 . In vitro, data of soft agar colony formation assay showed that colony formation rate in group A are significantly higher than group B (P < 0.01). 3. The collection and separation of A and B group in situ tumor cells, using flow cytometry instrument for in situ tumor cell side population quantitative analysis, group A compared with group B had obvious difference (P < 0.01). ConclusionThe knock out of the Galectin-3 gene reduces the skin cancer stem cells, inhibits tumor cell proliferation, depresses chemical carcinogenesis of mice skin. Galectin-3 gene may become the new target for skin cancer chemotherapy.

Key words: Tumor molecular targeted therapy , Galectin-3 , DMBA , TPA , Chemical carcinogenesis