DNA hypermethylation contributes to colorectal cancer metastasis by regulating the binding of CEBPB and TFCP2 to the CPEB1 promoter

Shao, Keke; Pu, Weilin; Zhang, Jianfeng; Guo, Shicheng; Qian, Fei; Glurich, Ingrid; Jin, Qing; Ma, Yanyun; Ju, Shaoqing; Zhang, Zhao; Ding, Weifeng

doi:10.1186/s13148-021-01071-z

Cited by 21 publications

(16 citation statements)

References 35 publications

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“…For example, CEBPB À/À mice are completely resistant to papilloma induced by chemical carcinogens [44], which was in accord with our report that silencing of CEBPB can increase ASS1 expression and alleviate the malignant biological behaviors and tumor progression. Indeed, CEBPB was identified to directly bind to the promoter of cytoplasmic polyadenylation element-binding protein 1, and thus, could inhibit transcription [45]. Veremeyko et al [46] showed that CEBPB is highly expressed in M1 macrophages, and it appears to inhibit Egr2, leading to loss of plasticity.…”

Section: Discussionmentioning

confidence: 99%

PGAM1 regulation of ASS1 contributes to the progression of breast cancer through the cAMP/AMPK/CEBPB pathway

Liu

Wang

et al. 2022

Molecular Oncology

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Phosphoglycerate mutase 1 (PGAM1) is a crucial glycolytic enzyme, and its expression status has been confirmed to be associated with tumor progression and metastasis. However, the precise role and other biological functions of PGAM1 remain unclear. Here, we report that PGAM1 expression is upregulated and related to poor prognosis in patients with breast cancer (BC). Functional experiments showed that knockdown of PGAM1 could suppress the proliferation, invasion, migration, and epithelial–mesenchymal transition of BC cells. Through RNA sequencing, we found that argininosuccinate synthase 1 (ASS1) expression was markedly upregulated in BC cells following PGAM1 knockdown, and it is required to suppress the malignant biological behavior of BC cells. Importantly, we demonstrated that PGAM1 negatively regulates ASS1 expression through the cAMP/AMPK/CEBPB axis. In vivo experiments further validated that PGAM1 promoted tumor growth in BC by altering ASS1 expression. Finally, immunohistochemical analysis showed that downregulated ASS1 levels were associated with PGAM1 expression and poor prognosis in patients with BC. Our study provides new insight into the regulatory mechanism of PGAM1‐mediated BC progression that might shed new light on potential targets and combination therapeutic strategies for BC treatment.

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Section: Discussionmentioning

confidence: 99%

PGAM1 regulation of ASS1 contributes to the progression of breast cancer through the cAMP/AMPK/CEBPB pathway

Liu

Wang

et al. 2022

Molecular Oncology

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“…Many pathways are associated with the pathogenesis of CD. [124], TLR8 [125], HTRA3 [126], CEBPB (CCAAT enhancer binding protein beta) [127], CD55 [128], CXCR2 [129], CCL28 [130], CBR3 [131], CCL3 [132], FCGR2A [48], ACSL1 [133], CCL2 [134], SOD2 [135], CD14 [136], IGFBP2 [137], CD274 [138], DERL3 [139], SERPINE1 [140], IDO1 [141], PDK1 [142] [156], TYMP (thymidine phosphorylase) [144], S100P [157], PDPN (podoplanin) [158], ADAMTS1 [159], ATF3 [160], TIMP1 [161], UCN2 [162], SELE (selectin E) [163], ICAM1 [164], FOSL1 [165], AREG (amphiregulin) [166], PIM2 [167], SLC7A5 [168], CH25H [169], COL5A2 [170], SNAI1 [171], MXRA5 [172], EGR1 [173], TNFRSF17 [174], MDFI (MyoD family inhibitor) [175], SRGN (serglycin) [176], CEACAM6 [177], CCL11 [178], IFNG (interferon gamma) [179], TREM2 [180], INHBA (inhibin subunit beta A) [181], APOE (apolipoprotein E) [182], FGR (FGR proto-oncogene, Src family tyrosine kinase) GBP5 [465], HGF (hepatocyte growth factor) [466], CXCL9 [467], SLC11A1 [468], IL1RN [469], STAT1 [470], CYP27B1 [471], MMP1 [472], SOCS3 [473], TLR8 [474], CD55 [475], CCL28 [476], FCGR2A [477], CCL2 [478],...…”

Section: Discussionmentioning

confidence: 99%

“…Signaling pathway include immune system [69], neutrophil degranulation [70], cytokine signaling in immune system [71], extracellular matrix organization [72], post-translational protein phosphorylation [73], biological oxidations [74], metabolism [75] and metabolism of lipids [76] were responsible for progression of CD. CXCL5 [77], CXCL3 [78], PROK2 [79], CXCR1 [80], PYCR1 [81], OSM (oncostatin M) [82], IL15RA [83], LRG1 [84], LCN2 [85], BATF2 [86], CXCL1 [87], S100A9 [88], IFITM1 [89], MYOF (myoferlin) [90], XBP1 [91], MMP3 [92], TAP1 [93], FPR2 [94], CXCL6 [95], C2CD4A [96], IFITM3 [97], IL1B [98], SLC6A14 [99], FPR1 [100], NOS2 [101], CHI3L1 [102], TGM2 [103], MUC4 [104], TREM1 [105], WNT5A [106], HGF (hepatocyte growth factor) [107], CXCL9 [108], GBP1 [109], S100A11 [110], ADM (adrenomedullin) [111], CXCL11 [112], CXCL10 [113], LILRB2 [114], GDF15 [115], IL1RN [116] STAT1 [117], SLAMF7 [105], CYP27B1 [118], NETO2 [119], TFPI2 [120], ZC3H12A [121], MMP1 [122], CSF3 [123], SOCS3 [124], TLR8 [125], HTRA3 [126], CEBPB (CCAAT enhancer binding protein beta) [127], CD55 [128], CXCR2 [129], CCL28 [130], CBR3 [131], CCL3 [132], FCGR2A [48], ACSL1 [133], CCL2 [134], SOD2 [135], CD14 [136], IGFBP2 [137], CD274 [138], DERL3 [139], SERPINE1 [140], IDO1 [141], PDK...…”

Section: Discussionmentioning

confidence: 99%

“…Many pathways are associated with the pathogenesis of CD. Signaling pathway include immune system [69], neutrophil degranulation [114], GDF15 [115], IL1RN [116] STAT1 [117], SLAMF7 [105], CYP27B1 [118], NETO2 [119], TFPI2 [120], ZC3H12A [121], MMP1 [122], CSF3 [123], SOCS3 [124], TLR8 [125], HTRA3 [126], CEBPB (CCAAT enhancer binding protein beta) [127], CD55 [128], CXCR2 [129], CCL28 [130], CBR3 [131], CCL3 [132], FCGR2A [48], ACSL1 [133], CCL2 [134], SOD2 [135] [150], CCR2 [151], VWF (von Willebrand factor) [152], SLC7A11 [153], NOD2 [154], DMBT1 [155], IL20RA [156], TYMP (thymidine phosphorylase) [144], S100P [157], PDPN (podoplanin) [158], ADAMTS1 [159], ATF3 [160], TIMP1 [161], UCN2 [162], SELE (selectin E) [163], ICAM1 [164], FOSL1 [165], AREG (amphiregulin) [166], PIM2 [167], SLC7A5 [168], CH25H [169], COL5A2 [170], SNAI1 [171], MXRA5 [172], EGR1 [173], TNFRSF17 [174], MDFI (MyoD family inhibitor) [175], SRGN (serglycin) [176], CEACAM6 [177], CCL11…”

Section: Discussionmentioning

confidence: 99%

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Identification of hub genes and key pathways in pediatric Crohn’s disease using next generation sequencing and bioinformatics analysis

Vastrad¹,

Vastrad²

2022

Preprint

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Pediatric Crohn's Disease (CD) also known as inflammatory bowel diseases, affects millions of people all over the world. The aim of this investigation is to identify the key genes in CD and uncover their potential functions. We downloaded the next generation sequencing (NGS) dataset GSE73374 from the Gene Expression Omnibus (GEO) database. The NGS dataset GSE73374 was used to screen differentially expressed genes (DEGs) between samples from patients with CD and healthy controls. Gene ontology (GO) and REACTOME pathway enrichment analyses were applied for the DEGs. Subsequently, a protein - protein interaction (PPI) network, modules, miRNA- hub gene regulatory network and TF - hub gene regulatory network were constructed to identify hub genes, miRNAs and TFs. Receiver operating characteristic curve (ROC) analysis was applied to validate the hub genes. A total of 957 DEGs were identified, including 478 up regulated genes and 479 down regulated genes. GO and REACTOME results suggested that several Go terms and pathways are involved in response to stimulus, extracellular region, signaling receptor binding, small molecule metabolic process, membrane, transporter activity, immune system and biological oxidations. The top centrality hub genes MDFI, MNDA, FBXO6, TFRC, STAT1, DPP4, MME, SLC39A4, APOA1 and TMEM25 were screened out as the critical genes among the DEGs from the PPI network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network. This investigation identified key genes and signal pathways, which might help us improve our understanding of the molecular mechanisms of CD and identify some novel therapeutic targets for CD.

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“…Furthermore, it has been demonstrated that CEBPB is the master regulator of macrophage differentiation, which could define the macrophage identity by marking the macrophage-specific chromatin regulatory elements for the following TF binding ( 21 ). The regulatory roles of CEBPB in the onset of cancer and the progression of its transcriptional regulatory function in malignant cells have also been uncovered ( 22 , 23 ). A few studies have also reported potential associations between CEBPB and metastasis ( 24 ) or treatment response in melanoma ( 25 ).…”

Section: Introductionmentioning

confidence: 99%

CEBPB is associated with active tumor immune environment and favorable prognosis of metastatic skin cutaneous melanoma

Yang

Xie

et al. 2022

Front. Immunol.

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Metastatic skin cutaneous melanoma (SKCM) is a common malignancy that accounts for low morbidity but high mortality of skin cancer. SKCM is characterized by high lymphocytic infiltration, whereas the states of infiltrated cells are variable in patients leading to a heterogeneous prognosis and hindering appropriate clinical decisions. It is therefore urgent to identify markers associated with lymphocytic infiltration, cellular conditions, and the prognosis of SKCM. In this study, we report that CEBPB, a transcriptional factor, is mainly expressed in macrophages in metastatic SKCM and associated with an active tumor immune environment and a favorable prognosis through integrated analysis of single-cell and bulk RNA-seq datasets. High CEBPB expression is significantly associated with active inflammation and immune response pathways in both macrophages and bulk SKCM tumor tissues. A signature based on CEBPB-associated genes that are specifically expressed in macrophages could robustly and prognostically separate different metastatic SKCM patients. In addition, the associations between the metastatic SKCM tumor signature and microenvironment with respect to T-cell recruitment and state, inflammation response, angiogenesis, and so on were also determined. In conclusion, we present here the first report on CEBPB in tumor immune environment and prognosis regulation in metastatic SKCM and construct a reliable signature, which should provide a useful biomarker for stratification of the patient’s prognosis and therapeutic selection.

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DNA hypermethylation contributes to colorectal cancer metastasis by regulating the binding of CEBPB and TFCP2 to the CPEB1 promoter

Cited by 21 publications

References 35 publications

PGAM1 regulation of ASS1 contributes to the progression of breast cancer through the cAMP/AMPK/CEBPB pathway

PGAM1 regulation of ASS1 contributes to the progression of breast cancer through the cAMP/AMPK/CEBPB pathway

Identification of hub genes and key pathways in pediatric Crohn’s disease using next generation sequencing and bioinformatics analysis

CEBPB is associated with active tumor immune environment and favorable prognosis of metastatic skin cutaneous melanoma

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