JMJD2A attenuation affects cell cycle and tumourigenic inflammatory gene regulation in lipopolysaccharide stimulated neuroectodermal stem cells

Das, Amitabh; Chai, Jin Choul; Jung, Kyoung Hwa; Das, Nando Dulal; Kang, Sung Chul; Lee, Young Seek; Seo, Hyemyung; Chai, Young Gyu

doi:10.1016/j.yexcr.2014.08.029

Cited by 14 publications

(14 citation statements)

References 56 publications

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“…Depletion of JMJD2A in the human lung cancer cell line A549 bearing an activated K-Ras allele triggered senescence ( Mallette and Richard, 2012 ). In addition, JMJD2A attenuation affected cell cycle and tumorigenic inflammatory gene regulation in neuroectodermal stem cells ( Das et al, 2014 ). In this study, our data indicated that JMJD2A was frequently over-expression in the lung cancer tissues and cell lines.…”

Section: Discussionsupporting

confidence: 54%

SIRT2 suppresses non-small cell lung cancer growth by targeting JMJD2A

Jiang

Shen

et al. 2015

Biological Chemistry

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Lung cancer has been the most prolific cancer in China - as in the rest of the world - with a high death rate and low 5-year survival rate. Previous evidence showed that JMJD2A is over-expressed in human non-small cell lung cancer (NSCLC) tissues compared to adjacent normal tissues, and that high level of JMJD2A predicts poor overall and disease-free survival. However, the mechanism by which JMJD2A is regulated in human NSCLC is not fully understood. In the present study, we identified that the SIRT2 as an anti-oncogenic protein in NSCLC was down-regulated. JMJD2A as a target of SIRT2 was negatively correlated with SIRT2 level in NSCLC. SIRT2 bound to the promoter region of JMJD2A and negatively regulated JMJD2A expression. In addition, we found that SIRT2 inhibited NSCLC cells proliferation, colony formation and tumor growth in vitro and in vivo in a JMJD2A-dependent manner. In summary, our findings implicate that SIRT2 suppresses non-small cell lung cancer growth through targeting JMJD2A and SIRT2 activator may serve as candidate drug for NSCLC therapy.

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Section: Discussionsupporting

confidence: 54%

SIRT2 suppresses non-small cell lung cancer growth by targeting JMJD2A

Jiang

Shen

et al. 2015

Biological Chemistry

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“…Recent studies have demonstrated that histone demethylases (kdm6b) and histone deacetylases (hdac1, hdac2, hdac3, and hdac7) potentially regulate proinflammatory gene expression in macrophages [ 44 , 65 , 66 ]. Recently, we showed that the histone demethylase kdm4a was significantly expressed in neuroectodermal stem cells and might play a role in tumorigenic development [ 35 ]. Interestingly herein, the RNA-Seq data also revealed that the histone demethylase Kdm4a and DNA methyltransferase Dnmt3l were strikingly differentially expressed in LPS-stimulated BV-2 microglial cells (Figs.…”

Section: Discussionmentioning

confidence: 99%

“…IPA (Ingenuity W Systems, http://www.ingenuity.com , Mountain View, CA, USA) was conducted to analyze the most significant canonical pathways in datasets as previously described [ 29 , 34 , 35 ]. Genes from datasets associated with canonical pathways in the Ingenuity Pathways Knowledge Base (IPAKB) were considered for literary analysis.…”

Section: Methodsmentioning

confidence: 99%

Dual RNA Sequencing Reveals the Expression of Unique Transcriptomic Signatures in Lipopolysaccharide-Induced BV-2 Microglial Cells

et al. 2015

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Microglial cells become rapidly activated through interactions with pathogens, and the persistent activation of these cells is associated with various neurodegenerative diseases. Previous studies have investigated the transcriptomic signatures in microglia or macrophages using microarray technologies. However, this method has numerous restrictions, such as spatial biases, uneven probe properties, low sensitivity, and dependency on the probes spotted. To overcome this limitation and identify novel transcribed genes in response to LPS, we used RNA Sequencing (RNA-Seq) to determine the novel transcriptomic signatures in BV-2 microglial cells. Sequencing assessment and quality evaluation showed that approximately 263 and 319 genes (≥ 1.5 log2-fold), such as cytokines and chemokines, were strongly induced after 2 and 4 h, respectively, and the induction of several genes with unknown immunological functions was also observed. Importantly, we observed that previously unidentified transcription factors (TFs) (irf1, irf7, and irf9), histone demethylases (kdm4a) and DNA methyltransferases (dnmt3l) were significantly and selectively expressed in BV-2 microglial cells. The gene expression levels, transcription start sites (TSS), isoforms, and differential promoter usage revealed a complex pattern of transcriptional and post-transcriptional gene regulation upon infection with LPS. In addition, gene ontology, molecular networks and pathway analyses identified the top significantly regulated functional classification, canonical pathways and network functions at each activation status. Moreover, we further analyzed differentially expressed genes to identify transcription factor (TF) motifs (−950 to +50 bp of the 5’ upstream promoters) and epigenetic mechanisms. Furthermore, we confirmed that the expressions of key inflammatory genes as well as pro-inflammatory mediators in the supernatants were significantly induced in LPS treated primary microglial cells. This transcriptomic analysis is the first to show a comparison of the family-wide differential expression of most known immune genes and also reveal transcription evidence of multiple gene families in BV-2 microglial cells. Collectively, these findings reveal unique transcriptomic signatures in BV-2 microglial cells required for homeostasis and effective immune responses.

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“…The overexpression of JMJD2A promotes the S phase and cancer cell proliferation, while depletion of JMJD2A suppresses cell growth in lung and bladder cancer cells (Kogure et al, 2013, Van Rechem, Black, 2011). JMJD2A attenuation affects cell cycle and tumourigenic inflammatory gene regulation in lipopolysaccharide syimulated neurodermal stem cells (Das et al, 2014), suggesting that FBXL4 could be involved in cell cycle through targeting JMJD2A.…”

Section: Roles Of Fbxl Sub-family In Cell Cyclementioning

confidence: 99%

Ubiquitination-mediated degradation of cell cycle-related proteins by F-box proteins

Zheng

Wang

Wei

2016

The International Journal of Biochemistry & Cell Biology

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F-box proteins, subunits of SKP1-cullin 1-F-box protein (SCF) type of E3 ubiquitin ligase complexes, have been validated to play a crucial role in governing various cellular processes such as cell cycle, cell proliferation, apoptosis, migration, invasion and metastasis. Recently, a wealth of evidence has emerged that F-box proteins is critically involved in tumorigenesis in part through governing the ubiquitination and subsequent degradation of cell cycle proteins, and dysregulation of this process leads to aberrant cell cycle progression and ultimately, tumorigenesis. Therefore, in this review, we describe the critical role of F-box proteins in the timely regulation of cell cycle. Moreover, we discuss how F-box proteins involve in tumorigenesis via targeting cell cycle-related proteins using biochemistry studies, engineered mouse models, and pathological gene alternations. We conclude that inhibitors of F-box proteins could have promising therapeutic potentials in part through controlling of aberrant cell cycle progression for cancer therapies.

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JMJD2A attenuation affects cell cycle and tumourigenic inflammatory gene regulation in lipopolysaccharide stimulated neuroectodermal stem cells

Cited by 14 publications

References 56 publications

SIRT2 suppresses non-small cell lung cancer growth by targeting JMJD2A

SIRT2 suppresses non-small cell lung cancer growth by targeting JMJD2A

Dual RNA Sequencing Reveals the Expression of Unique Transcriptomic Signatures in Lipopolysaccharide-Induced BV-2 Microglial Cells

Ubiquitination-mediated degradation of cell cycle-related proteins by F-box proteins

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