Fig. 6: Snail-CHST2 axis mediated breast cancer cell migration by enhanced MECA79 antigen synthesis.

A FACS analysis of MDA-MB-231-pLU-Vector (black) and MDA-MB-231-pLU-Snail (red) cells stained by MECA79 mAb, left panel: Representative histograms were shown. Right panel: MFI of MECA79 antigen synthesis by breast cancer cells was shown compared with the vector group. Data were shown as mean ± SD from three independent experiments. *P < 0.05, Student t test. B MECA79 surface expression in MDA-MB-7-pLU-Vector (black) cells and MCF-7-pLU-Snail cells with CHST2 knockdown was assessed by flow cytometry, left panel: Representative histograms were shown. Right panel: MFI of MECA79 antigen synthesis by cancer cells was shown compared with Snail group. Data were shown as mean ± SD, three independent experiments were performed. **P < 0.01, *P < 0.05, Student t test. C, D Transwell assays in MDA-MB-231-Vector or MCF-7-Vector and MDA-MB-231-Snail cells or MCF-7-Snail cells with MECA79 or isotype antibody treated (left panels), six fields chosen randomly were counted for statistical analysis (right panels) and data were shown as mean ± SD of three independent experiments, **P < 0.01, *P < 0.05. Student t test. E Schematic model for the role of Snail-CHST2-MECA79 sulfation axis in breast cancer cell migration and metastasis. Snail activated transcription of CHST2 via binding to promoter sequences, and simultaneously induced CHST2 expression which increased sulfation level in MECA79 antigen synthesis to enhance migration and metastasis of breast cancer cells. Furthermore, blocking cell surface MECA79 antigen inhibited cancer cell migration.