Specificity Protein 1 (Sp1) Maintains Basal Epithelial Expression of the miR-200 Family

Kolesnikoff, Natasha; Attema, Joanne L.; Roslan, Suraya; Bert, Andrew G.; Schwarz, Quenten; Gregory, Philip A.; Goodall, Gregory J.

doi:10.1074/jbc.m113.529172

Cited by 62 publications

(60 citation statements)

References 70 publications

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“…Members of the miR-200 family are downregulated during progression and migration of ovarian and breast cancer, as well as in bladder, pancreatic, prostate and esophageal carcinoma. Furthermore, in several of these entities, downregulation of miR-200 is associated with reduced overall survival and poor response to chemotherapy (28)(29)(30)(31)(32)(33)(34)(35). In the present study, we found that HCC patients with low miR-200a expression had significantly worse prognosis than those with high expression of miR-200a.…”

Section: Discussionsupporting

confidence: 54%

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

et al. 2014

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Abstract. miR-200a suppresses tumor development and progression; however, its role in tumor growth and metastasis of hepatocellular carcinoma (HCC) and the underlying mechanism have not been elucidated. In the present study, we identified that miR-200a was markedly downregulated in HCC and exerted suppressive effects on tumor cell growth and metastasis. We identified that miR-200a suppressed tumor growth and metastasis by directly targeting MACC1. In addition, HCC patients with low miR-200a expression had significantly worse prognosis than those with high expression of miR-200a. These findings suggest that miR200a may be recognized as a novel potential biomarker to predict the survival of patients with HCCs following liver transplantation.

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Section: Discussionsupporting

confidence: 54%

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

et al. 2014

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“…Our findings added additional miRNA targets regulated by JUN and SP1 in response to KRAS activation, which helped to elucidate the mechanism of JUN and SP1 in mediating KRAS functions. Interestingly, SP1 has been reported to activate mir-200 expression only in epithelial cells but not in mesenchymal cell types (55), strongly suggesting that SP1 may cooperate with different cofactors to affect mir-200 expression differently in distinct cellular contexts.…”

Section: Discussionmentioning

confidence: 99%

Suppression of MicroRNA 200 Family Expression by Oncogenic KRAS Activation Promotes Cell Survival and Epithelial-Mesenchymal Transition in KRAS-Driven Cancer

Zhong

Zheng

Shen

et al. 2016

Molecular and Cellular Biology

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T he cellular oncogene KRAS encodes two splice isoforms, KRAS4A and the predominant form KRAS4B (here referred to as KRAS), which is a small GTPase that links extracellular stimuli to intracellular signaling pathways regulating developmental processes and diseases, especially cancers (1-5). KRAS protein has been widely reported to bear activating mutations (e.g., G12D, G13D, and Q61L) in cancers derived from lung, colon, and pancreas (1-5). These mutations impair the GTPase activity of KRAS and enable constitutive activation of downstream pathways independent of exogenous regulatory signals. The abnormal activation of downstream effectors in KRAS pathways, such as RAF-extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3K)/AKT, had been found to contribute to KRASdriven tumorigenesis, which is characterized by cellular transformation, resistance to apoptosis, and metastasis (1-6). Moreover, downstream transcription factors of KRAS pathways, such as FOS, JUN, nuclear factor B (NF-B), and Fra1, are required for cancer cell survival, proliferation, migration, and invasion (7-10). Although the molecular mechanisms dictating how the aberrant activation of KRAS pathways affects transformed phenotypes and tumorigenesis have been well studied, the role of noncoding genes in mediating KRAS function is still largely unknown (11).MicroRNAs (miRNAs) are endogenous 18-to 25-nucleotide noncoding small RNAs that regulate gene expression in a sequence-specific manner via the degradation of target mRNAs or inhibition of protein translation (12)(13)(14). MicroRNA 200 (mir-200) is a well-characterized, highly conserved miRNA family, consisting of five members that are located in two miRNA gene clusters (mir-200b/a/429 and mir-200c/141) on different chromosomes. Each cluster is transcribed into a single primary miRNA transcript (pri-miRNA) and processed by the Drosha/ DGCR8 complex into individual precursor transcripts (premiRNA), which are further sliced by Dicer into mature miRNAs. The five mature miRNAs of the family contain highly similar seed sequences, which leads them to share a wide range of biological functions, such as regulation of development (15-17), cellular senescence (18), apoptosis (19), tumor metastasis (20-27), angiogenesis (28), and immunosuppression of lymphocytes (29). These biological functions of mir-200 were disclosed by the discovery of its target genes, such as those coding for ZEB1/2 (21, 22, 24-26), SEC23 (30), CXCL1/IL-8 (28), and PD-L1 (29), in different cellular contexts. Similar to other miRNAs involved in tumorigenesis (31), the expression levels of mir-200 family members were deregulated in cancer cells by different mechanisms, implying their crit-

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“…In the kidney the transcriptional regulation by HNF-1␤ appears to be specific to the miR-200b/a/429 cluster as the levels of the miR-200c/141 cluster are unchanged in HNF-1␤ mutant cells or kidneys. The promoters of the human miR-200b/a/429 and miR-200c/141 clusters have been characterized (41,42), and transcription factors that regulate expression have been identified, including Sp1, the p53/p63/p73 family, and c-Myb (43)(44)(45). These transcription factors may contribute to the residual expression of the miR-200 cluster observed in HNF-1␤ mutant cells and kidneys (Fig.…”

Section: Discussionmentioning

confidence: 99%

Transcription Factor Hepatocyte Nuclear Factor-1β (HNF-1β) Regulates MicroRNA-200 Expression through a Long Noncoding RNA

Hajarnis

Patel

Aboudehen

et al. 2015

Journal of Biological Chemistry

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Specificity Protein 1 (Sp1) Maintains Basal Epithelial Expression of the miR-200 Family

Cited by 62 publications

References 70 publications

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

Suppression of MicroRNA 200 Family Expression by Oncogenic KRAS Activation Promotes Cell Survival and Epithelial-Mesenchymal Transition in KRAS-Driven Cancer

Transcription Factor Hepatocyte Nuclear Factor-1β (HNF-1β) Regulates MicroRNA-200 Expression through a Long Noncoding RNA

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