The mechanism of SP1/p300 complex promotes proliferation of multiple myeloma cells through regulating IQGAP1 transcription

Jin, Zhouxiang; Zhou, Shujuan; Ye, Haige; Jiang, Songfu; Kang, Yu; Ma, Ying

doi:10.1016/j.biopha.2019.109434

Cited by 17 publications

(9 citation statements)

References 42 publications

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“…At this stage, consistent with previous data, we correlated the MM-EV miRNA content with the dimished Sp1 levels in hMSC. To date, Sp1 expression was correlated to MM cell proliferation [75,76] but its expression in hMSC during MM bone disease development still need to be explored.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicle microRNAs Contribute to the Osteogenic Inhibition of Mesenchymal Stem Cells in Multiple Myeloma

Raimondo

Urzì

Conigliaro

et al. 2020

Cancers

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Osteolytic bone disease is the major complication associated with the progression of multiple myeloma (MM). Recently, extracellular vesicles (EVs) have emerged as mediators of MM-associated bone disease by inhibiting the osteogenic differentiation of human mesenchymal stem cells (hMSCs). Here, we investigated a correlation between the EV-mediated osteogenic inhibition and MM vesicle content, focusing on miRNAs. By the use of a MicroRNA Card, we identified a pool of miRNAs, highly expressed in EVs, from MM cell line (MM1.S EVs), expression of which was confirmed in EVs from bone marrow (BM) plasma of patients affected by smoldering myeloma (SMM) and MM. Notably,we found that miR-129-5p, which targets different osteoblast (OBs) differentiation markers, is enriched in MM-EVs compared to SMM-EVs, thus suggesting a selective packaging correlated with pathological grade. We found that miR-129-5p can be transported to hMSCs by MM-EVs and, by the use of miRNA mimics, we investigated its role in recipient cells. Our data demonstrated that the increase of miR-129-5p levels in hMSCs under osteoblastic differentiation stimuli inhibited the expression of the transcription factor Sp1, previously described as a positive modulator of osteoblastic differentiation, and of its target the Alkaline phosphatase (ALPL), thus identifying miR-129-5p among the players of vesicle-mediated bone disease.

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Section: Discussionmentioning

confidence: 99%

Extracellular Vesicle microRNAs Contribute to the Osteogenic Inhibition of Mesenchymal Stem Cells in Multiple Myeloma

Raimondo

Urzì

Conigliaro

et al. 2020

Cancers

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“…4). Many studies have shown the interaction of Sp1 with p300 within the same regulatory complex on promoters of genes which they regulate, such as p21 59 , IL-12 60 , and IQGAP 61 . The presence of p300 allows for assembly of the transcription complex in which it acts as a bridging factor to connect transcription factors to the basal transcription machinery, but also leads to targeted histone acetylation to open up the chromatin environment and to¨bookmark¨the promoters for rapid transcription Fig.…”

Section: Discussionmentioning

confidence: 99%

Dissecting myogenin-mediated retinoid X receptor signaling in myogenic differentiation

et al. 2020

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Deciphering the molecular mechanisms underpinning myoblast differentiation is a critical step in developing the best strategy to promote muscle regeneration in patients suffering from muscle-related diseases. We have previously established that a rexinoid x receptor (RXR)-selective agonist, bexarotene, enhances the differentiation and fusion of myoblasts through a direct regulation of MyoD expression, coupled with an augmentation of myogenin protein. Here, we found that RXR signaling associates with the distribution of myogenin at poised enhancers and a distinct E-box motif. We also found an association of myogenin with rexinoid-responsive gene expression and identified an epigenetic signature related to histone acetyltransferase p300. Moreover, RXR signaling augments residue-specific histone acetylation at enhancers co-occupied by p300 and myogenin. Thus, genomic distribution of transcriptional regulators is an important designate for identifying novel targets as well as developing therapeutics that modulate epigenetic landscape in a selective manner to promote muscle regeneration.

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“…Therefore, we believed that the overexpression of COL1A2 in GC was caused by the coordination between EP300 and TWIST1. A similar mechanism was observed in multiple myeloma cells as well where SP1/EP300 complex promoted proliferation of cancer cells through modulating the transcription of IQGAP1 [24]. Furthermore, Asano and Trojanowska reported that Fli1 recruited HDAC1/EP300 to the COL1A2 promoter and suppressed the expression of 10 Analytical Cellular Pathology the COL1A2 through histone deacetylation in human dermal fibroblasts [25].…”

Section: Discussionmentioning

confidence: 53%

TWIST1-EP300 Expedites Gastric Cancer Cell Resistance to Apatinib by Activating the Expression of COL1A2

Chen

et al. 2022

Analytical Cellular Pathology

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The association between collagen type I alpha (COL1A) and chemoresistance has been verified in cancers. However, the specific role of COL1A2 in gastric cancer (GC) cell resistance to apatinib, a highly selective small-molecule inhibitor of vascular endothelial growth factor receptor 2, has not been investigated before. The purpose of this study was to explore the potential factors associated with COL1A2 regulation on GC cell apatinib resistance in vitro. With the aid of the Oncomine database and integrated bioinformatics methods, we identified COL1A2 overexpression in GC and its prognostic value. Mechanistically, the COL1A2 promoter has a distinct H3K27ac modification site and that E1A binding protein p300 (EP300) and twist family bHLH transcription factor 1 (TWIST1) can bind to the COL1A2 promoter, which in turn transcriptionally activated COL1A2 expression. In addition, overexpression of COL1A2 significantly promoted resistance to apatinib in GC cells, but knockdown of EP300 or TWIST1 remarkably inhibited COL1A2 expression and promoted sensitivity of GC cells to apatinib. Our findings demonstrated that the combination of EP300 and TWIST1 has a synergistically regulatory effect on COL1A2 expression, thus contributing to apatinib resistance in GC cells.

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The mechanism of SP1/p300 complex promotes proliferation of multiple myeloma cells through regulating IQGAP1 transcription

Cited by 17 publications

References 42 publications

Extracellular Vesicle microRNAs Contribute to the Osteogenic Inhibition of Mesenchymal Stem Cells in Multiple Myeloma

Extracellular Vesicle microRNAs Contribute to the Osteogenic Inhibition of Mesenchymal Stem Cells in Multiple Myeloma

Dissecting myogenin-mediated retinoid X receptor signaling in myogenic differentiation

TWIST1-EP300 Expedites Gastric Cancer Cell Resistance to Apatinib by Activating the Expression of COL1A2

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