Intronic miR-26b controls neuronal differentiation by repressing its host transcript,<i>ctdsp2</i>

Dill, Holger; Linder, Bastian; Fehr, Alexander; Fischer, Utz

doi:10.1101/gad.177774.111

Cited by 119 publications

(113 citation statements)

References 35 publications

(43 reference statements)

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“…Many studies have demonstrated that miRNAs can function as oncogenes or tumor suppressors, and are often dysregulated in tumors (31). miRNAs play a vital role in many crucial cellular processes, including apoptosis, differentiation, invasion, and proliferation (32)(33)(34). The abnormal expression of miRNA has been reported in many cancers, including breast (35), gastric (36), colorectal (37), and liver cancers (38), as well as leukemia (39) and lymphoma (40).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

Sun

et al. 2016

Oncology Reports

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Abstract. MicroRNA (miRNA) is a type of endogenous non-coding RNA implicated in various cellular processes. Studies have shown that miR-124 is involved in the malignant progression of cancer, but little is known concerning its potential role in breast cancer. Therefore, the purpose of this study was to conduct a functional analysis of miR-124 in breast cancer, and to identify its target genes in this disease. To this end, we used quantitative real-time PCR to examine the expression level of miR-124 in breast cancer tissue specimens and cell lines. To study the functional significance of miR-124, we overexpressed miR-124 with miR-124 mimics and observed breast cancer cell proliferation, colony formation, migration, and invasion abilities by in vitro cell culture experiments. Target prediction algorithms and luciferase reporter gene assays were used to identify the target genes of miR-124. We also knocked down miR-124 targets using short hairpin RNA (shRNA) constructs, and observed associated breast cancer cell characteristics by in vitro cell culture experiments. We found that miR-124 expression significantly decreased in breast cancer tissues and cells compared to normal tissues and cells. In addition, cell proliferation, colony formation, migration, and invasion were decreased after overexpression of miR-124 in breast cancer cells. Furthermore, we used several algorithms to identify the snail family zinc finger 2 (SNAI2) as a potential target gene of miR-124. The protein expression level and luciferase activity of the 3'-untranslated region of SNAI2 were significantly decreased in breast cancer cells transfected with miR-124 mimics. Cell proliferation, colony formation, migration, and invasion were also decreased after knockdown of SNAI2 by shRNA. In conclusion, our data suggest that miR-124 expression is decreased in breast cancer and plays an important role as a tumor suppressor gene by targeting SNAI2. These findings may reveal novel perspectives for clinical treatments against breast cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

Sun

et al. 2016

Oncology Reports

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“…For example, Kloting et al (14) isolated miRNA from different fat depots of overweight and obese individuals in 2009 and Zhao et al (22) profiled 220 miRNAs in pancreatic islets, adipose tissue and liver isolated from diabetes-resistant (B6) and diabetes-susceptible (BTBR) mice. miR-26b is an intronic miRNA located in the intron of the CTDSP1 gene, which is able to regulate its host transcript (23). Emerging evidence has indicated that miR-26b is associated with the development of obesity.…”

Section: Discussionmentioning

confidence: 99%

Expression of microRNA-26b, an obesity-related microRNA, is regulated by free fatty acids, glucose, dexamethasone and growth hormone in human adipocytes

Xu¹,

Shi

et al. 2014

Molecular Medicine Reports

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Abstract. MicroRNAs (miRNAs) are short non-coding RNAs that are involved in numerous biological processes, including obesity and insulin resistance. miR-26b is an obesity-related intronic miRNA located in the intron of the carboxy-terminal domain, RNA polymerase II, polypeptide A, small phosphatase 1 gene. miR-26b is abundantly expressed in mice and mature human adipocytes, and is associated with the expression of adipokines. In the present study, the effects of energy-source materials and hormones associated with obesity, on miR-26b expression were investigated. It was demonstrated that free fatty acids (FFAs), glucose, glucocorticoids and growth hormone (GH) downregulate the expression of miR-26b in human adipocytes. The results indicate that the expression of miR-26b is affected by a variety of factors that are correlated with obesity and insulin sensitivity. Therefore, miR-26b may be an important mediator in the development of obesity-associated insulin resistance.

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“…Recently, it was determined that miR-34a is involved in NSC differentiation; miR-34a promotes Notch signaling by repressing Numbl, a negative regulator of Notch signaling that inhibits neuronal differentiation [110] . Additionally, miR-26b activates neurogenesis by suppressing Ctdsp2 protein expression [111,112] . By targeting Nestin, miR-125b promotes NSPC differentiation and migration while inhibiting NSPC proliferation [113] (Figure 2).…”

Section: Neuronal Differentiationmentioning

confidence: 99%

MicroRNAs as novel regulators of stem cell fate

Choi

Hwang³

2013

WJSC

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Mounting evidence in stem cell biology has shown that microRNAs (miRNAs) play a crucial role in cell fate specification, including stem cell self-renewal, lineagespecific differentiation, and somatic cell reprogramming. These functions are tightly regulated by specific gene expression patterns that involve miRNAs and transcription factors. To maintain stem cell pluripotency, specific miRNAs suppress transcription factors that promote differentiation, whereas to initiate differentiation, lineagespecific miRNAs are upregulated via the inhibition of transcription factors that promote self-renewal. Small molecules can be used in a similar manner as natural miRNAs, and a number of natural and synthetic small molecules have been isolated and developed to regulate stem cell fate. Using miRNAs as novel regulators of stem cell fate will provide insight into stem cell biology and aid in understanding the molecular mechanisms and crosstalk between miRNAs and stem cells.Ultimately, advances in the regulation of stem cell fate will contribute to the development of effective medical therapies for tissue repair and regeneration. This review summarizes the current insights into stem cell fate determination by miRNAs with a focus on stem cell self-renewal, differentiation, and reprogramming. Small molecules that control stem cell fate are also highlighted.© 2013 Baishideng. All rights reserved. Key words:MicroRNA; Stem cell fate; Differentiation; Self-renewal; Reprogramming; Small molecule Core tip: Stem cells are important in regenerative medicine applications due to their capacity to self-renew and differentiate into specific cell types. MicroRNAs (miRNAs) are short non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. Recent studies suggest that miRNAs are key molecules in the regulation of stem cell fate decisions; this regulation is manifested as the fine tuning of cell-and tissue-specific gene expression. This review summarizes the current insights into stem cell fate determination by miRNAs and focuses on stem cell self-renewal, differentiation, and reprogramming. Small molecules that control stem cell fate are also highlighted.

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Intronic miR-26b controls neuronal differentiation by repressing its host transcript,ctdsp2

Cited by 119 publications

References 35 publications

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

Expression of microRNA-26b, an obesity-related microRNA, is regulated by free fatty acids, glucose, dexamethasone and growth hormone in human adipocytes

MicroRNAs as novel regulators of stem cell fate

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