Menin Is Required for Optimal Processing of the MicroRNA let-7a

Gurung, Buddha; Muhammad, Abdul Bari; Hua, Xianxin

doi:10.1074/jbc.m113.520692

Cited by 23 publications

(29 citation statements)

References 55 publications

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“…Remarkably, Vijayaraghavan and colleagues observed that in MIN6 and betalox5 cells, miR‐24 binding to menin mRNA leads to cellular proliferation and improves cell viability . In addition, growing grounds demonstrate that menin plays a decisive role in the processing of certain miRNAs . Taken as a whole, these data point to the existence of a bidirectional crosstalk between miRNA processing and β‐cell development, and further highlight the complexity of the miRNA network involved in pancreas development.…”

Section: Mirnas and The Development Of β‐Cellsmentioning

confidence: 95%

Shaping and preserving β‐cell identity with microRNAs

Dumortier

Fabris

Obberghen

2016

Diabetes Obesity Metabolism

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The highly sophisticated identity of pancreatic β-cells is geared to accomplish its unique feat of providing insulin for organismal glucose and lipid homeostasis. This requires a particular and streamlined fuel metabolism which defines mature β-cells as glucose sensors linked to an insulin exocytosis machinery. The establishment of an appropriate β-cell mass and function during development as well as the maintenance of their identity throughout life are necessary for energy homeostasis. The small non-coding RNAs, microRNAs (miRNAs), are now wellrecognized regulators of gene transcripts, which in general are negatively affected by them.Convincing evidence exists to view miRNAs as major actors in β-cell development and function, suggesting an important role for them in the distinctive β-cell 'identity card'. Here, we summarize key features that associate miRNAs and the establishment of the appropriate β-cell identity and its necessary maintenance during their 'long life'. K E Y W O R D Sβ-cell development, β-cell identity, insulin secretion, microRNAs, type 2 diabetes | INTRODUCTIONThe identity of cells is defined by the expression of a particular set of genes and the resulting production of specific proteins and constituents depending on them. These expression patterns follow a complex scenario during cell development, where timing and quantity of the proteins produced are essential and finely regulated. The maintenance of these distinctive cell identities throughout life is required for normal physiology and health of the organism.In mammals, β-cells are the major cell type within the pancreatic islets. In humans, they represent nearly 60% of the islet cells.1 They are the unique source of circulating insulin, the chief anabolic hormone. Indeed, insulin is critically important for fuel homeostasis and energy storage. Concerning glucose homeostasis, β-cells serve as a glucostat in a highly sophisticated homeostatic feedback system.

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Section: Mirnas and The Development Of β‐Cellsmentioning

confidence: 95%

Shaping and preserving β‐cell identity with microRNAs

Dumortier

Fabris

Obberghen

2016

Diabetes Obesity Metabolism

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“…Besides this, genes known to be crucial for parathyroid cell proliferation and hormonal activity regulate miRNA expression in non-parathyroid cells: in the thick ascending limb of Henle, CASR activation by extracellular calcium regulates the expression of miR-9 and miR-374, which in turn inhibit the expression of claudin 14-mediated ultrafiltrated calcium reabsorption [32]; in ectopically expressing menin HEK293 and MEF cells, menin interacts with arsenite-resistant protein 2 (ARS2), a component of the nuclear RNA CAP-binding complex that is crucial for biogenesis of certain miRNAs including let-7a and miR-155 [33]. Therefore, data produced in non-parathyroid cells suggest that the products of the key genes of parathyroid tumours (CASR and menin) modulate the expression of miRNAs that in turn might contribute to the phenotype of parathyroid neoplasia.…”

Section: Micrornas and Potential Gene Targets In Parathyroid Tumoursmentioning

confidence: 99%

MicroRNA deregulation in parathyroid tumours suggests an embryonic signature

Verdelli

Forno

Vaira

et al. 2015

J Endocrinol Invest

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Primary hyperparathyroidism is a common endocrine disorder caused by abnormal tumour parathyroid cell proliferation. Parathyroid tumours show a great variability both in clinical features, such as the severity of PTH secretion, the rate and the pattern of cell proliferation, and genetic background. Studies aiming to develop new diagnostic markers and therapeutic approaches need a deeper definition of this variability. Dysregulation of microRNAs (miRNAs) has been shown to play an essential role in the development and progression of cancer. MiRNAs are small noncoding RNAs that inhibit the translation and stability of messenger RNAs (mRNAs). Here, data about the miRNA expression pattern in parathyroid normal and tumour glands were reviewed. Though available data in parathyroid tumours are very limited, the expression pattern of a subset of specific miRNAs clearly discriminated parathyroid carcinomas from normal parathyroid glands and, more clinically relevant, from parathyroid adenomas. Investigation showed that parathyroid tumours were characterized by an embryonic expression pattern of miRNAs such as miR-296, or the miRNA clusters C19MC and miR-371-3, typically in stem cells committed to differentiation or during human embryonic development, respectively. Further, miRNA profiles were correlated with tumour aggressive behaviour. Moreover, the interaction with the oncosuppressor menin suggests that miRNAs might modulate the function of the known oncosuppressors or oncogenes involved in parathyroid tumourigenesis and thus overseeing the tumour phenotype. In conclusion, miRNAs might provide new diagnostic markers and new therapeutic approaches by developing molecular miRNA-targeted therapies for the cure of parathyroid tumours, whose unique option is surgery.

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“…Menin does not affect levels of primary-let-7a (pri-let-7a), but increases the levels of mature let-7a (Gurung et al 2014). Let-7a targets, including insulin receptor (INSR) and insulin receptor substrate 2 (IRS2), pro-proliferative genes that are crucial for insulin-mediated signaling, are up-regulated in Men1 -excised cells (Gurung et al 2014). Inhibition of let-7a using anti-miRNA in wild type cells is sufficient to enhance the expression of IRS2.…”

Section: Introductionmentioning

confidence: 98%

“…We previously found that menin interacts with arsenite-resistant protein 2 (ARS2), a component of the nuclear RNA CAP-binding complex that is crucial for biogenesis of certain miRNAs including let-7a (Gurung, et al 2014). Menin does not affect levels of primary-let-7a (pri-let-7a), but increases the levels of mature let-7a (Gurung et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic regulation by the menin pathway

Feng¹,

Ma²,

Hua³

2017

Endocrine-Related Cancer

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There is a trend of increasing prevalence of neuroendocrine tumors (NETs), and the inherited multiple endocrine neoplasia type 1 (MEN1) syndrome serves as a genetic model to investigate how NETs develop and the underlying mechanisms. Menin, encoded by the MEN1 gene, at least partly acts as a scaffold protein by interacting with multiple partners to regulate cellular homeostasis of various endocrine organs. Menin has multiple functions including regulating several important signaling pathways by controlling gene transcription. Here, we focus on reviewing the recent progress in elucidating the key biochemical role of menin in epigenetic regulation of gene transcription and cell signaling, as well as posttranslational regulation of menin itself. In particular, we will review the progress in studying structural and functional interactions of menin with various histone modifiers and transcription factors such as MLL, PRMT5, SUV39H1 and other transcription factors including c-Myb and JunD. Moreover, the role of menin in regulating cell signaling pathways such as TGF-beta, Wnt, and Hedgehog, as well as miRNA biogenesis and processing will be described. Further, the regulation of the MEN1 gene transcription, posttranslational modifications and stability of menin protein will be reviewed. These various modes of regulation by menin as well as regulation of menin by various biological factors broaden the view regarding how menin controls various biological processes in neuroendocrine organ homeostasis.

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Menin Is Required for Optimal Processing of the MicroRNA let-7a

Cited by 23 publications

References 55 publications

Shaping and preserving β‐cell identity with microRNAs

Shaping and preserving β‐cell identity with microRNAs

MicroRNA deregulation in parathyroid tumours suggests an embryonic signature

Epigenetic regulation by the menin pathway

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