Regulation of transcription factor suppresses malignant properties of cancer cells with changes in glycosylation

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In this grant, we established the Sp1-knockdown cells from A549 human lung carcinoma cells by RNAi technique, and examined the relationship between protein glycosylation and malignant properties. Lectin blot analysis showed that decreased galactosylation of N-glycans is observed for E-cadherin in the Sp1-knockdown cells. The gene expression level of beta-1,4-GalT I decreased significantly by knockdown of Sp1. Analysis of the promoter region of the human beta-1,4-GalT I gene revealed that the Sp1-binding site are critical for the expression of the gene. Moreover, knockdown of Sp1 resulted in suppression of the tumorigenic potential and migratory activity of A549 cells. Furthermore, the EGF receptor signaling was reduced by knockdown of Sp1. The study indicates that the malignant properties of cancer cells can be suppressed by regulating Sp1 through changes in protein glycosylation, and suggests that Sp1 may be a potential target for cancer therapy.