| First Author | Yasmeen R | Year | 2013 |
| Journal | Biochim Biophys Acta | Volume | 1833 |
| Issue | 12 | Pages | 3218-3227 |
| PubMed ID | 24080087 | Mgi Jnum | J:204057 |
| Mgi Id | MGI:5529541 | Doi | 10.1016/j.bbamcr.2013.09.012 |
| Citation | Yasmeen R, et al. (2013) Aldehyde dehydrogenase-1a1 induces oncogene suppressor genes in B cell populations. Biochim Biophys Acta 1833(12):3218-27 |
| abstractText | The deregulation of B cell differentiation has been shown to contribute to autoimmune disorders, hematological cancers, and aging. We provide evidence that the retinoic acid-producing enzyme aldehyde dehydrogenase 1a1 (Aldh1a1) is an oncogene suppressor in specific splenic IgG1(+)/CD19(-) and IgG1(+)/CD19(+) B cell populations. Aldh1a1 regulated transcription factors during B cell differentiation in a sequential manner: 1) retinoic acid receptor alpha (Rara) in IgG1(+)/CD19(-) and 2) zinc finger protein Zfp423 and peroxisome proliferator-activated receptor gamma (Pparg) in IgG1(+)/CD19(+) splenocytes. In Aldh1a1(-/-) mice, splenic IgG1(+)/CD19(-) and IgG1(+)/CD19(+) B cells acquired expression of proto-oncogenic genes c-Fos, c-Jun, and Hoxa10 that resulted in splenomegaly. Human multiple myeloma B cell lines also lack Aldh1a1 expression; however, ectopic Aldh1a1 expression rescued Rara and Znf423 expressions in these cells. Our data highlight a mechanism by which an enzyme involved in vitamin A metabolism can improve B cell resistance to oncogenesis. |
