Upregulation of Cyclin B1 by miRNA and its implications in cancer

Huang, Vera; Place, Robert F.; Portnoy, Victoria; Wang, Ji; Qi, Zhongxia; Jia, Zhejun; Yu, Angela; Shuman, Marc A.; Yu, Jingwei; Li, Long Cheng

doi:10.1093/nar/gkr934

Cited by 255 publications

(266 citation statements)

References 62 publications

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“…24,25 Most recently, cyclinB1 was shown to be upregulated by miR-744 and miR-1186, prolonged overexpression of which causes CIN and inhibits tumour growth. 26 Central to mitosis is SAC, which monitors accurate chromosome segregation. Although Mad1, Mad2, BubR1/Mad3 and Bub3 are major SAC components, they have been joined by players like Cdc20, Bub1, Mps1 and AuroraB.…”

Section: Discussionmentioning

confidence: 99%

miR-125b promotes cell death by targeting spindle assembly checkpoint gene MAD1 and modulating mitotic progression

et al. 2012

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The spindle assembly checkpoint (SAC) is a 'wait-anaphase' mechanism that has evolved in eukaryotic cells in response to the stochastic nature of chromosome-spindle attachments. In the recent past, different aspects of the SAC regulation have been described. However, the role of microRNAs in the SAC is vaguely understood. We report here that Mad1, a core SAC protein, is repressed by human miR-125b. Mad1 serves as an adaptor protein for Mad2 -which functions to inhibit anaphase entry till the chromosomal defects in metaphase are corrected. We show that exogenous expression of miR-125b, through downregulation of Mad1, delays cells at metaphase. As a result of this delay, cells proceed towards apoptotic death, which follows from elevated chromosomal abnormalities upon ectopic expression of miR-125b. Moreover, expressions of Mad1 and miR-125b are inversely correlated in a variety of cancer cell lines, as well as in primary head and neck tumour tissues. We conclude that increased expression of miR-125b inhibits cell proliferation by suppressing Mad1 and activating the SAC transiently. We hypothesize an optimum Mad1 level and thus, a properly scheduled SAC is maintained partly by miR-125b.

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Section: Discussionmentioning

confidence: 99%

miR-125b promotes cell death by targeting spindle assembly checkpoint gene MAD1 and modulating mitotic progression

et al. 2012

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“…A number of documentation showed that, less RNAPII (RNA polymerase II) is available at promoter region after TGS [40,42,44,[46][47][48][49][50][51] where as there is an enrichment of RNAPII in case of RNA [50,[52][53][54]. Studies have reported modified histones enriched promoters having well known silencing marks after TGS and active marks just after RNAa.…”

Section: Argonate Protein In Transcription Machinery and Epigenetic Rmentioning

confidence: 99%

“…Nuclear function of AGO proteins also reported as a regulator of transcriptional gene silencing (TGS) in fission yeast and plants. Nuclear role of mammalian AGO proteins include gene activation [52,60,65], TGS [57,[66][67][68] and alternative splicing [64] (Figure 3). AGO1 and AGO2 both play an important role in neuronal differentiation by miRNA-mediated process [69] through binding with the same pool of miRNAs and mRNA targets [70].…”

Section: Argonate Protein In Transcription Machinery and Epigenetic Rmentioning

confidence: 99%

“…Similarly, to induce histone and DNA methylation Argonaute proteins interact with ribonucleoprotein complexes in plant [87]. In mammals, AGO members are associated with a spectrum of nuclear processes including gene activation [10,52,60,65], TGS [57,[66][67][68] and alternative splicing [64]. Further, the direct interaction of nuclear AGO1 with RNA Polymerase II (RNAPII) and subsequent wide association with chromosomal loci of the transcriptionally active gene's promoter region has been elicited by ChIP-seq analysis.…”

Section: Function Of Ago-1 During Tumor Formationmentioning

confidence: 99%

“…Deletion of the PAZ domain which functions as RNA-binding domain in AGO1, interfered with gene activation; further suggesting a role of RNAs (miRNA) in this process. Exogenous miRNA transfection can promote AGO1 enrichment at highly-complementary sites of gene promoters to control transcription of those genes [51,52,57]. In context of AGO1-RNAP II association, formation of a duplex with complementary target sequence may be plays a role to load AGO1 with miRNA which protects bound RNA from RNase (RNase A/T1) digestion, similar to canonical target recognition manner [116,117].…”

Section: Function Of Ago-1 During Tumor Formationmentioning

confidence: 99%

See 2 more Smart Citations

Argonaute-1 Machinery Silent Cancer Noises

Mondal¹,

Pal²,

Bhadra³

et al. 2017

Cancer Surg

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Small non-coding RNA mediated that is micromanaging of global gene regulation was well established as fundamental principle in cell or tissue functions. To carry out, biological role small RNA needs a unique batch of protein family named Argonaute (AGO). The Argonaute proteins carry sophisticated and highly delicate interacting modules common for three specialized small RNAs, microRNA (miRNA), short interfering RNA (siRNA) and Piwi interacting RNA (piRNA). These RNA-proteins complexes are unique to coordinate silencing events in the genome. Recent works have made a novel role of AGO1 protein by extending its tentacle towards cancer monitoring pathways. It makes a constructive bridge between a direct and constructive link between cancer and RNAi (RNA interference) machinery. Apart from multifarious classical functions such as disruption of mRNA translation, decay, transcriptional regulation and splicing, we demonstrate a new concept to narrate the role of AGO1 proteins in different cancer regulatory pathways via microRNA-Argonaute circuit specifically.

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Mouse‐specific up‐regulation of Ccnb1 expression by miR‐199a‐5p in keratinocyte

Kim

Lee

et al. 2016

FEBS Open Bio

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MicroRNA (miRNA) are a class of single‐stranded, small non‐coding RNA that regulate various biological processes, including skin and hair cycle regulation, by modulating the expression of specific genes at the post‐transcriptional level. Recently, several studies reported that miRNA directly or indirectly up‐regulate target genes. Previously, we performed microarray analysis to identify the target genes of miR‐199a‐5p in a mouse skin keratinocyte cell line and detected more than 200 genes whose expression was significantly increased by miR‐199a‐5p overexpression (> 1.5‐fold). In this study, we further investigated these genes and found that cyclin B1 (Ccnb1) expression was positively regulated by miR‐199a‐5p in keratinocyte. Moreover, Ccnb1 expression was inversely correlated with miR‐199a‐5p expression during the mouse hair cycle. Cell cycle analysis showed that the proportion of cells in S phase was slightly increased, while the proportion of cells in G2/M phase decreased by miR‐199‐5p. Using luciferase assay, we found that the 3′ untranslated region of Ccnb1 was a direct target of miR‐199a‐5p. We also found that the regulation of Ccnb1 expression by miR‐199a‐5p is mouse specific. CCNB1 expression was not affected in the human and monkey cell lines. These results provide a new relationship between Ccnb1 and miR‐199a‐5p in both mouse keratinocyte and miRNA biology.

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Upregulation of Cyclin B1 by miRNA and its implications in cancer

Cited by 255 publications

References 62 publications

miR-125b promotes cell death by targeting spindle assembly checkpoint gene MAD1 and modulating mitotic progression

miR-125b promotes cell death by targeting spindle assembly checkpoint gene MAD1 and modulating mitotic progression

Argonaute-1 Machinery Silent Cancer Noises

Mouse‐specific up‐regulation of Ccnb1 expression by miR‐199a‐5p in keratinocyte

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