Loss of PRDM11 promotes MYC-driven lymphomagenesis

Fog, Cathrine K.; Asmar, Fazila; Côme, Christophe; Jensen, Kjeld Truberg; Johansen, Jens Vilstrup; Kheir, Tony Bou; Jacobsen, Linda; Friis, Carsten; Louw, Alison; Rosgaard, Louise; Øbro, Nina Friesgaard; Marquart, Hanne Vibeke; Anthonsen, Kristian; Braat, Arie Koen; Lohuizen, Maarten van; Ralfkiær, Elisabeth; Grønbæk, Kirsten; Lund, Anders H.

doi:10.1182/blood-2014-03-560805

Cited by 19 publications

(22 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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 ].…”

Section: Other Prdms As Tumor Suppressors In Cancermentioning

confidence: 99%

See 1 more Smart Citation

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

Mzoughi

Tan

Low

et al. 2016

Current Opinion in Genetics & Development

View full text Add to dashboard Cite

Section: Other Prdms As Tumor Suppressors In Cancermentioning

confidence: 99%

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

Section: Prdm11mentioning

confidence: 99%

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

Mzoughi

Tan

Low

et al. 2016

Current Opinion in Genetics & Development

View full text Add to dashboard Cite

“…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 …”

mentioning

confidence: 99%

PRDM8 exhibits antitumor activities toward hepatocellular carcinoma by targeting NAP1L1

Chen

Gao

et al. 2018

Hepatology

View full text Add to dashboard Cite

show abstract

“…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 …”

Section: Introductionmentioning

confidence: 99%

“…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.…”

Section: Introductionmentioning

confidence: 99%

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

Zhou¹,

Chen²,

et al. 2019

Cancer Medicine

View full text Add to dashboard Cite

PRDM family proteins are dysregulated in many human diseases, especially hematological malignancies and solid cancers, and share a unique N‐terminal PR domain followed by zinc fingers toward the C terminus. With a high frequency of DNA promoter hypermethylation, PRDM5 is primarily considered as a tumor suppressor in solid tumors. However, little is known about the function of PRDM5 in blood malignancies, especially acute myeloid leukemia (AML). In this study, we showed that high PRDM5 expression levels were independently correlated with poor overall survival in AML patients. PRDM5 overexpression promoted cell proliferation, colony formation, and migration in vitro and enhanced tumorigenesis in an in vivo xenograft model. Furthermore, we found that PRDM5 overexpression promoted cell cycle progression with the decreased level of cell cycle inhibitors such as p16 and p21, and regulated the expression of epithelial‐mesenchymal transition markers ZO‐1 and Vimentin to promote migration. Moreover, we observed that PRDM5 upregulated the Jun N‐terminal kinase (JNK) signaling pathway and downregulated c‐Myc expression. Pharmacological inhibition of JNK by SP600125 partially abrogated PRDM5‐induced cell proliferation and migration. Taken together, our findings demonstrate that PRDM5 functions as an oncogenic driver in AML via JNK pathway, suggesting that PRDM5 is a potential therapeutic target for AML.

show abstract

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.

Cited by 19 publications

References 51 publications

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

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

PRDM8 exhibits antitumor activities toward hepatocellular carcinoma by targeting NAP1L1

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

Contact Info

Product

Resources

About