Zhu et al. Journal of Experimental & Clinical Cancer Research 2012, 31:31 http://www.jeccr.com/content/31/1/31 Page 4 of 7 Figure 1 Expressions of BLyS, TACI, BCMA and BAFF-R in human breast cancer cell lines. (A) BLyS and its three receptors in human breast cancer cell lines MDA-MB-435, MDA-MB-231, MDA-MB-468 and B cell line Ramos by immunofluorescence (original magnification 200 ×) and Western Blotting. (B) The mRNA level of BLyS in the three cell lines were detected by real-time PCR under hypoxia for different time points. Data were means of triplicate samples with ± SD; vs normoxia, *, P < 0.05; **, P < 0.01; ***, P < 0.001. (C) BLyS protein level in MDA-MB-435 cells by Western Blotting analysis. Enhanced migration of MDA-MB-435 cells in response to BLyS or 2% FBS was blocked by SB 202190 and/or API-1 (Figure 4A). MDA-MB-435 cells were treated with BLyS for 4 h, which led to the maximal phosphory- lation levels of Akt protein (Figure 4B). As shown in Figure 4C, BLyS-induced phosphorylations of Akt could be abrogated by the specific inhibitors. But phosphoryla- tion level of p38 MAPK induced by BLyS did not increase significantly as compared to the control. It suggested that inhibition by SB 202190 could be through another mechanism and BLyS-independent. In short, BLyS probably promoted breast cancer cell migra- tion via Akt pathways. Discussion We initially demonstrated that hypoxia modulated the expressions of BLyS and its receptors in human breast cancer cell lines. Our data also indicated enhanced