Tumor Suppressive Function of mir-205 in Breast Cancer Is Linked to HMGB3 Regulation

Elgamal, Ola A.; Park, Jong Kook; Gusev, Yuriy; Azevedo-Pouly, Ana Clara P.; Jiang, Jinmai; Roopra, Avtar; Schmittgen, Thomas D.

doi:10.1371/journal.pone.0076402

Cited by 93 publications

(79 citation statements)

References 30 publications

(38 reference statements)

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“…Recent study of Nemeth et al [39] showed that HMGB3 played a key role in regulating the balance between proliferation and differentiation in the primitive stages of hematopoiesis. Overexpression of HMGB3 has been found in metastatic breast cancers [40]. In this study, HMGB3 was significantly enriched in GO terms associated with negative regulation of cell differentiation.…”

Section: Discussionsupporting

confidence: 52%

Genes and pathways identified in thyroid carcinoma based on bioinformatics analysis

Yu¹,

Mai²,

Cui³

et al. 2016

neo

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The objective of this study was to investigate the key genes and pathways associated with thyroid carcinoma. Based on the microarray data of GSE27155, we identified the differentially expressed genes (DEGs) between four types of thyroid carcinoma samples (papillary carcinoma (PTC), oncocytic carcinoma (OTC), follicular carcinoma (FTC) and anaplastic carcinoma (ATC)) and normal controls. With the obtained DEGs, we performed gene functional interaction (FI) network analysis. Then we conducted Venn diagram analysis to identify the intersection and specific DEGs of the four types of thyroid carcinomas. The intersections DEGs were performed by functional enrichment and transcription factor (TF) prediction analyses. These specific DEGs were performed by pathway enrichment analysis. There were respectively 323, 318, 118 and 1005 DEGs identified in PTC, OTC, FTC and ATC. Twelve sub-network modules were extracted based on gene FI network analysis and eight thyroid carcinoma-associated DEGs were involved in the network, such as TIMP1. Based on the Venn diagram analysis, 27 common DEGs were identified, such as HMGB3 which was regulated by TF of NKX3-1. There were 149 PTC-specific DEGs (like CLDN1), 160 OTC-specific DEGs, 94 FTC-specific DEGs (like PPARG), and 789 ATC-specific DEGs (like CDK1). They were enriched in some pathways, such as Cell cycle, Citrate cycle, and Oxidative phosphorylation. TIMP1, HMGB3, CLDN1, CDK1 and PPARG as well as pathways of Cell cycle, Citrate cycle, and Oxidative phosphorylation may play important roles in the progression of thyroid carcinoma.

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Section: Discussionsupporting

confidence: 52%

Genes and pathways identified in thyroid carcinoma based on bioinformatics analysis

Yu¹,

Mai²,

Cui³

et al. 2016

neo

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“…Concordant with our data, Want et al recently implicated miR-320 in chemo-sensitivity by targeting FOXM1 in vitro , a critical gene which plays a principle role in colon, lung, and breast cancer tumor initiation and progression [26–28]. Similarly, other investigators have also shown that FOXQ1 played a key role in nasopharyngeal carcinoma, targeted by miR-506 and miR-124 [29, 30]; likewise, HMGB3 in breast cancer is targeted by miR-205 [31]; and MKI67 in hepatocellular carcinoma, targeted by miR-519d [32]. …”

Section: Discussionmentioning

confidence: 99%

MicroRNA-320 suppresses colorectal cancer by targeting SOX4, FOXM1, and FOXQ1

et al. 2016

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Colorectal cancer (CRC) is the third most common cancer causing high mortality rates world-wide. Delineating the molecular mechanisms leading to CRC development and progression, including the role of microRNAs (miRNAs), are currently being unravelled at a rapid rate. Here, we report frequent downregulation of the microRNA miR-320 family in primary CRC tissues and cell lines. Lentiviral-mediated re-expression of miR-320c (representative member of the miR-320 family) inhibited HCT116 CRC growth and migration in vitro, sensitized CRC cells to 5-Fluorouracil (5-FU), and inhibited tumor formation in SCID mice. Global gene expression analysis in CRC cells over-expressing miR-320c, combined with in silico prediction identified 84 clinically-relevant potential gene targets for miR-320 in CRC. Using a series of biochemical assays and functional validation, SOX4, FOXM1, and FOXQ1 were validated as novel gene targets for the miR-320 family. Inverse correlation between the expression of miR-320 members with SOX4, FOXM1, and FOXQ1 was observed in primary CRC patients' specimens, suggesting that these genes are likely bona fide targets for the miR-320 family. Interestingly, interrogation of the expression levels of this gene panel (SOX4, FOXM1, and FOXQ1) in The Cancer Genome Atlas (TCGA) colorectal cancer data set (319 patients) revealed significantly poor disease-free survival in patients with elevated expression of this gene panel (P-Value: 0.0058). Collectively, our data revealed a novel role for the miR-320/SOX4/FOXM1/FOXQ1 axes in promoting CRC development and progression and suggest targeting those networks as potential therapeutic strategy for CRC.

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“…HMGB3 protein is highly expressed in the embryo and hardly detectable in adult tissues (Vaccari et al, 1998). HMGB3 expression is regulated by several miRNAs, including miR-206, miR-205, miR-10A, and miR-21 (Elgamal et al, 2013; Maciotta et al, 2012; Zhu et al, 2013c). HMGB3 −/− mice are viable and HMGB3 is required for eye and brain development (Terada et al, 2006).…”

Section: Introduction and Historical Backgroundmentioning

confidence: 99%

“…The formation of HMGB3-NPU98 fusion protein is a new oncogene identified in leukemia and significantly promotes malignant transformation in recipient mice (Petit et al, 2010). HMGB3 overexpression is associated with progression and poor prognosis of solid tumors such as breast, gastric, and non-small cell lung cancers (Elgamal et al, 2013; Gong et al, 2013; Song et al, 2013). However, the effect of HMGB3 in tumor therapy and the extracellular role of HMGB3 remain unknown.…”

Section: Introduction and Historical Backgroundmentioning

confidence: 99%

HMGB1 in health and disease

Kang

Chen

Zhang

et al. 2014

Molecular Aspects of Medicine

801

828

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Complex genetic and physiological variations as well as environmental factors that drive emergence of chromosomal instability, development of unscheduled cell death, skewed differentiation, and altered metabolism are central to the pathogenesis of human diseases and disorders. Understanding the molecular bases for these processes is important for the development of new diagnostic biomarkers, and for identifying new therapeutic targets. In 1973, a group of non-histone nuclear proteins with high electrophoretic mobility was discovered and termed High-Mobility Group (HMG) proteins. The HMG proteins include three superfamilies termed HMGB, HMGN, and HMGA. High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside the cell as the prototypic damage associated molecular pattern molecule (DAMP). This DAMP, in conjunction with other factors, thus has cytokine, chemokine, and growth factor activity, orchestrating the inflammatory and immune response. All of these characteristics make HMGB1 a critical molecular target in multiple human diseases including infectious diseases, ischemia, immune disorders, neurodegenerative diseases, metabolic disorders, and cancer. Indeed, a number of emergent strategies have been used to inhibit HMGB1 expression, release, and activity in vitro and in vivo. These include antibodies, peptide inhbitiors, RNAi, anti-coagulants, endogenous hormones, various chemical compounds, HMGB1-receptor and signaling pathway inhibition, artificial DNAs, physical strategies including vagus nerve stimulation and other surgical approaches. Future work further investigating the details of HMGB1 localizationtion, structure, post-translational modification, and identifccation of additional partners will undoubtedly uncover additional secrets regarding HMGB1’s multiple functions.

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Tumor Suppressive Function of mir-205 in Breast Cancer Is Linked to HMGB3 Regulation

Cited by 93 publications

References 30 publications

Genes and pathways identified in thyroid carcinoma based on bioinformatics analysis

Genes and pathways identified in thyroid carcinoma based on bioinformatics analysis

MicroRNA-320 suppresses colorectal cancer by targeting SOX4, FOXM1, and FOXQ1

HMGB1 in health and disease

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