miR-200b targets GATA-4 during cell growth and differentiation

Yao, Chunxia; Wei, Qingxia; Zhang, Yanyan; Wang, Weiping; Xue, Lixiang; Yang, Fen; Zhang, Shufeng; Xiong, Cheng-Juan; Li, Wenyan; Wei, Zhiru; Zou, Yunzeng; Zang, Ming-Xi

doi:10.4161/rna.24370

Cited by 46 publications

(37 citation statements)

References 29 publications

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“…More recently, Yao et al demonstrated that miR-200b was a critical regulator of the zinc finger transcription factor GATA-4, which regulates the expression of CCND1 at the transcriptional level. Their results supported that miR-200b could regulate tumor cell growth and differentiation by targeting GATA-4 to downregulate the expression of CCND1 [77]. Thus, these findings support that miR-200 can exert control over the cell cycle at many levels through the modulation of several different factors.…”

Section: Tumor Suppressive Signatures Of Mir-200mentioning

confidence: 63%

MiR-200, a new star miRNA in human cancer

et al. 2014

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MicroRNAs (miRNAs) are a set of non-coding small RNA molecules in control of gene expression at posttranscriptional/translational level. They not only play crucial roles in normal developmental progress, but also are commonly dysregulated in human diseases, including cancer. MiR-200 is a family of tumor suppressor miRNAs consisting of five members, which are significantly involved in inhibition of epithelial-to-mesenchymal transition (EMT), repression of cancer stem cells (CSCs) self-renewal and differentiation, modulation of cell division and apoptosis, and reversal of chemoresistance. In this article, we summarize the latest findings with regard to the tumor suppressor signatures of miR-200 and the regulatory mechanisms of miR-200 expression. The collected evidence supports that miR-200 is becoming a new star miRNA in study of human cancer.

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Section: Tumor Suppressive Signatures Of Mir-200mentioning

confidence: 63%

MiR-200, a new star miRNA in human cancer

et al. 2014

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“…Recent reports indicated that miRNA-200b is highly correlated with cell proliferation222425. Especially, in cardiac cell lines, Yao et al 31. demonstrated that miR-200b overexpression inhibited the cell growth and downregulated the expression of cyclin D1 and myosin heavy chain (MHC) by regulating the expression of GATA-4.…”

Section: Discussionmentioning

confidence: 99%

Cardiac repair in a mouse model of acute myocardial infarction with trophoblast stem cells

Chen

Zhang

et al. 2017

Sci Rep

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Various stem cells have been explored for the purpose of cardiac repair. However, any individual stem cell population has not been considered as the ideal source. Recently, trophoblast stem cells (TSCs), a newly described stem cell type, have demonstrated extensive plasticity. The present study evaluated the therapeutic effect of TSCs transplantation for heart regeneration in a mouse model of myocardial infarction (MI) and made a direct comparison with the most commonly used mesenchymal stem cells (MSCs). Transplantation of TSCs and MSCs led to a remarkably improved cardiac function in contrast with the PBS control, but only the TSCs exhibited the potential of differentiation into cardiomyocytes in vivo. In addition, a significantly high proliferation level of both transplanted stem cells and resident cardiomyocytes was observed in the TSCs group. These findings primary revealed the therapeutic potential of TSCs in transplantation therapy for MI.

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“…Overexpression of miR99a attenuated Nodal signaling via repression of Smarca5 chromatin remodeling activity and cardiac gene promoters were shown to have increased H3K27me3 levels. A variety of additional studies have functionally confirmed miRNA roles in pluripotent-CM differentiation including miR199a-3p, miR590-3p (91), miR363 (Gupta and Rao, 2014), miR499 miR200b (Yao et al, 2013), miR1, miR499 (Fu et al, 2011), andmiR-133 (Takaya et al, 2009). However, additional work will be needed to determine ncRNA control of and regulation by, other epigenetic regulators of chromatin architecture through CM differentiation.…”

Section: Epigenetics Of Pluripotent-cm Differentiationmentioning

confidence: 93%

An epigenetic perspective on the failing heart and pluripotent-derived-cardiomyocytes for cell replacement therapy

Tompkins

Riggs

2014

Front. Biol.

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As life expectancy rises, the prevalence of heart failure is steadily increasing, while donors for organ transplantation remain in short supply (Zwi-Dantsis and Gepstein, 2012). Indeed, myocardial infarction represents the foremost cause of death within industrialized nations (Henning, 2011) and further, approximately 1% of all newborns harbor a congenital heart defect. Although medical interventions allow > 80% of those with cardiac defects to survive to adulthood, there are often extreme emotional and financial burdens that accompany such congenital anomalies, and many individuals will remain at a heightened risk for myocardial infarction throughout the remainder of their lives (Verheugt et al., 2010;Amianto et al., 2011). In this review, we will discuss the nature of the failing heart and strategies for repair from an epigenetic standpoint. Significant focus will reside on pluripotent-to-cardiomyocyte differentiation for cell replacement, epigenetic mechanisms of cardiomyocyte differentiation, epigenetic "memories," and epigenetic control of cardiomyocyte cell fate toward translational utility.

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miR-200b targets GATA-4 during cell growth and differentiation

Cited by 46 publications

References 29 publications

MiR-200, a new star miRNA in human cancer

MiR-200, a new star miRNA in human cancer

Cardiac repair in a mouse model of acute myocardial infarction with trophoblast stem cells

An epigenetic perspective on the failing heart and pluripotent-derived-cardiomyocytes for cell replacement therapy

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