Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple myeloma (MM) results from biased proliferation of cancerous plasma cells (PC). Therapeutic strategies that target MM PC will provide immense value to the treatment of MM. For this, it is necessary to identify novel molecules that differ between MM PC and healthy PC. RNA sequencing was used to determine differences in gene expression profiles between LPS-induced plasmablasts (PB)/PC and the PB-like myeloma SP 2/0 cell line. Compared to LPS-induced PB/PC, SP 2/0 cells expressed significantly lower levels of Loc108167440 mRNA. Loc108167440 overexpression reduced the number of SP 2/0 cells by stimulating apoptotic cell death. In addition, Loc108167440 overexpression suppressed tumor progression in the SP 2/0 xenograft mouse model. Finally, we demonstrated that Loc108167440 overexpression up-regulated expression of p53 in SP 2/0 cells. These results suggest that Loc108167440 overexpression suppressed SP 2/0 cell growth by inducing p53-mediated apoptosis. Thus, Loc108167440 overexpression may be a potential therapy for treating MM.
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PMID:Loc108167440 suppressed myeloma cell growth by P53-mediated apoptosis. 3094 84

Proper expression of the transcription factor, Positive regulatory domain 1 (PRDM1), is required for maintaining homeostasis of human monocyte derived-dendritic cells (MO-DCs). The molecular mechanisms and gene targets of PRDM1 in B and T lymphocytes have been identified. However, the function of PRDM1 in dendritic cells (DCs) remains unclear. We investigate co-regulators of PRDM1 in MO-DCs identified by mass spectrometry (MS) and co-immunoprecipitation (Co-IP). Notably, non-POU domain-containing octamer-binding protein (NonO) was found to be a PRDM1 binding protein in the nucleus of MO-DCs. NonO is recruited to the PRDM1 binding site in the promoter region of IL-6. Knockdown of NonO expression by siRNA lessened suppression of IL-6 promoter activity by PRMD1 following LPS stimulation. While NonO binding to PRDM1 was observed in human myeloma cell lines, an effect of NonO on IL-6 expression was not observed. Thus, loss of NonO interrupted the inhibitory effect of PRDM1 on IL-6 expression in MO-DCs, but not plasma cells. Moreover, MO-DCs with low expression of PRDM1 or NonO induce an increased number of IL-21-producing TFH-like cells in vitro. These data suggest that low level of PRDM1 and NonO lead to enhanced activation of MO-DCs and the regulation of MO-DC function by PRDM1 is mediated through cell lineage-specific mechanisms.
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PMID:NonO Is a Novel Co-factor of PRDM1 and Regulates Inflammatory Response in Monocyte Derived-Dendritic Cells. 3276 3


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