Loss of PRDM11 promotes MYC-driven lymphomagenesis

Abstract

Key Points Loss of Prdm11 accelerates MYC-driven lymphomagenesis. PRDM11 regulates transcription of target genes, including FOS and JUN.

The role of PRDMs in cancer: one family, two sides

“…Deletion of PRDM11 accelerated Myc-driven lymphomagenesis, while its overexpression induced apoptosis and delayed lymphoma onset. Mechanistically, PRDM11 seems to directly regulate expression of oncogenes such as Fos (FBJ Murine Osteosarcoma Viral Oncogene Homolog) and Jun (V-Jun Avian Sarcoma Virus 17 Oncogene Homolog) [49 ].…”

“…Tumor suppressor: deletion accelerated Myc-driven lymphomagenesis, while overexpression induced apoptosis and delayed lymphoma onset [49].…”

PRDM8 exhibits antitumor activities toward hepatocellular carcinoma by targeting NAP1L1

“…Overexpression of PRDM5 in cancer cells induces cell cycle arrest and apoptosis. PRDM11 overexpression induces apoptosis and delayed lymphoma onset . PRDM12 exerts an antiproliferative effect on chronic myeloid leukemia …”

Overexpression of PRDM5 promotes acute myeloid leukemia cell proliferation and migration by activating the JNK pathway

“…PRDM3 (MDS1‐EVI1) is critical for the initiation and progression of MLL‐AF9‐induced AML. In prostatic cancers, PRDM16S (MEL1S) is overexpressed and has an antiapoptotic function …”

“…In prostatic cancers, PRDM16S (MEL1S) is overexpressed and has an antiapoptotic function. [5][6][7][8][9] PRDM5 (or PFM2) is a recently identified member of the PRDM protein family and is located at human chromosome region 4q26, which harbors many tumor suppressor genes active in several cancers. 10 PRDM5 participates in inducing committed murine blood cells to differentiate into hematopoietic stem cells and modulates the transcription of a subset of developmental regulators during mouse embryonic stem cell differentiation.…”