Diabetes mellitus potentiates diffuse large B-cell lymphoma via high levels of CCL5.

There is much evidence suggesting that CCL5 is one of the chemoattractant cytokines involved in diabetes mellitus (DM) with diffuse large B-cell lymphoma (DLBCL). However, the pathological impact is unclear. In the current study, in order to improve understanding regarding the role of CCL5 in DM with DLBCL, the expression levels of CCL5 mRNA were examined in normal B cells, human DLBCL cell lines (Ly1, Ly8 and Ly10) and a mouse DLBCL cell line (A20), as well as those in cells cultured with either 5 or 30 mmol/l glucose. A20-CCL5+ (CCL5 overexpression) and A20-CCL5- (CCL5 knockdown) subclones were obtained through cell transduction with a lentiviral vector, and were subcutaneously injected into BALB/c DM mice and normal mice. Tumor growth was observed by calculating the tumor volume. The results demonstrated that CCL5 mRNA levels in DLBCL cells were significantly higher than those in the normal cells (P<0.05); and levels in DLBCL cells in 30 mmol/l Glu were significantly higher than in those of DLBCL cells in 5 mmol/l Glu (P<0.05). A20-CCL5+ cells led to tumor formation in DM mice compared with A20 and A20-CCL5- cells. These results indicate that high levels of CCL5 expression may accelerate DLBCL formation in DM. [ABSTRACT FROM AUTHOR]