| First Author | Liu J | Year | 2019 |
| Journal | Immunology | Volume | 156 |
| Issue | 1 | Pages | 56-68 |
| PubMed ID | 30171602 | Mgi Jnum | J:269342 |
| Mgi Id | MGI:6259969 | Doi | 10.1111/imm.12998 |
| Citation | Liu J, et al. (2019) Deceleration of glycometabolism impedes IgG-producing B-cell-mediated tumor elimination by targeting SATB1. Immunology 156(1):56-68 |
| abstractText | B lymphocytes, known as antibody producers, mediate tumor cell destruction in the manner of antibody-dependent cell-mediated cytotoxicity; however, their anti-tumor function seems to be weakened during tumorigenesis, while the underlying mechanisms remain unclear. In this study, we found that IgG mediated anti-tumor effects, but IgG-producing B cells decreased in various tumors. Considering the underlying mechanism, glycometabolism was noteworthy. We found that tumor-infiltrating B cells were glucose-starved and accompanied by a deceleration of glycometabolism. Both inhibition of glycometabolism and deprivation of glucose through tumor cells, or glucose-free treatment, reduced the differentiation of B cells into IgG-producing cells. In this process, special AT-rich sequence-binding protein-1 (SATB1) was significantly silenced in B cells. Down-regulating SATB1 by inhibiting glycometabolism or RNA interference reduced the binding of signal transducer and activator of transcription 6 (STAT6) to the promoter of germline Cgamma gene, subsequently resulting in fewer B cells producing IgG. Our findings provide the first evidence that glycometabolic inhibition by tumorigenesis suppresses differentiation of B cells into IgG-producing cells, and altering glycometabolism may be promising in improving the anti-tumor effect of B cells. |
