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Inhibiting PRDM5 expression by siRNA attenuated the IFN-gamma-triggered accumulation of active caspase-3 and cleaved PARP in intestinal epithelial cells. Moreover, flow cytometry assay and CCK-8 analysis revealed that PRDM5 knockdown significantly alleviated the IFN-gamma-induced cellular apoptosis in HT29 cells.
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Both Prdm 4 and Prdm 5 are expressed in human corneal endothelium, primary hCECs and in HCECs-12 cells, characterised by expression of the Na(+)/K(+)-ATPase.
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The miR-182 promoter is rarely methylated in epithelial ovarian cancers (EOCs), and its methylation status is associated with lower miR-182 expression. Deletion of the PRDM5 locus may play a supportive role in miR-182 overexpression in EOC. miR-182 is an unfavorable prognostic factor in EOC.
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The current study revealed a novel mutation in the PRDM5 gene in a Brittle cornea syndrome (BCS) family and recurrent mutation in a sporadic BCS patient.
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Genetic variants in PRDM5 can lead to various syndromic and nonsyndromic disorders affecting the anterior segment of the eye.
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Defective interaction of PRDM5 with repressive complexes, and dysregulation of H3K9me2, play a role in PRDM5-associated disease.
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Reduced expression of PRDM5 was observed in the cornea and retina of brittle cornea syndrome patients.
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These data suggest that PRDM5 is a relevant tumour suppressor gene that is frequently targeted in colorectal tumourigenesis.
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PRDM2, PRDM5, PRDM16 promoters are methylated and their expression is suppressed in lung cancer cells.
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Data provide the first causal link between Prdm5 loss and intestinal carcinogenesis, and uncover an extensive and novel PRDM5 target repertoire likely facilitating the tumor-suppressive functions of PRDM5.
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Promoter methylation-mediated downregulation of PRDM5 contributes to the development of lung squamous cell carcinoma.
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Frequent epigenetic silencing of PRDM5 is involved in multiple tumorigeneses, which could serve as a tumor biomarker
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ZNF469 and PRDM5, two genes that when mutated cause brittle cornea syndrome, participate in the same regulatory pathway.
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Data show that reduced expression of PRDM5 may play an important role in the pathogenesis and/or development of cervical cancer, and is considered to be caused in part by aberrant DNA methylation.
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PRDM5 caused G2/M arrest and apoptosis upon infection of tumor cells. These results suggest that inactivation of PRDM5 may play a role in carcinogenesis.
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Results identify PRDM5, which acts as a sequence-specific, DNA binding transcription factor that targets hematopoiesis-associated protein-coding and microRNA genes, some of which are targets of Gfi1.
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Data suggest that epigenetic alteration of PRDM5 (e.g., methylation of its 5'-CpG island or trimethylation of Lys(27) of histone H3) likely plays a key role in the progression of gastrointestinal cancers and may be a useful molecular marker.
