MiR-29 Induces K562 Cell Apoptosis by Down-Regulating FoxM1

Wang, Xiaofang; Zhong, Hua; Wang, Lei; Dong, Youhai; Jia, Ai‐Qun; Mo, Qingjiang; Zhang, Chenguang

doi:10.12659/msm.894554

Cited by 10 publications

(8 citation statements)

References 19 publications

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“…A literature examination of many of these differentially regulated miRNAs shed some light on their known roles, and many were found to contribute to the formation and/or function of the nervous system (Table 1). Many of these miRNAs also exhibited overlapping cellular functions, contributing to processes such as tumorigenesis [23][24][25][26][27][28][29][30], differentiation [31][32][33], proliferation [34][35][36][37][38], apoptosis [39][40][41][42], and cell cycle regulation [34,43,44]. A subset of the miRNAs was associated with nervous system-specific processes, such as differentiation [45][46][47][48][49], lifespan [50], neurite guidance [51][52][53], or synaptogenesis [54][55][56].…”

Section: Identification Of Mirnas That Were Differentially Regulated mentioning

confidence: 99%

Identification and Characterization of microRNAs during Retinoic Acid-Induced Regeneration of a Molluscan Central Nervous System

Walker

Spencer

Necakov

et al. 2018

Preprint

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Retinoic acid (RA) is the biologically active metabolite of vitamin A and has become a well-established factor that induces neurite outgrowth and regeneration in both vertebrates and invertebrates. However, the underlying regulatory mechanisms that may mediate RA-induced neurite sprouting remain unclear. In the past decade, microRNAs have emerged as important regulators of nervous system development and regeneration, and have been shown to contribute to processes such as neurite sprouting. However, few studies have demonstrated the role of miRNAs in RA-induced neurite sprouting. By miRNA sequencing analysis, we identify 482 miRNAs in the regenerating central nervous system (CNS) of the mollusc Lymnaea stagnalis, 219 of which represent potentially novel miRNAs. Of the remaining conserved miRNAs, 38 show a statistically significant up-or downregulation in regenerating CNS as a result of RA treatment. We further characterized the expression of one neuronally-enriched miRNA upregulated by RA, miR-124. We demonstrate, for the first time, that miR-124 is expressed within the cell bodies and neurites of regenerating motorneurons. Moreover, we identify miR-124 expression within the growth cones of cultured ciliary motorneurons (pedal A), whereas expression in the growth cones of another class of respiratory motorneurons (right parietal A) was absent in vitro. These findings support our hypothesis that miRNAs are important regulators of retinoic acid-induced neuronal outgrowth and regeneration in regeneration-competent species.

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Section: Identification Of Mirnas That Were Differentially Regulated mentioning

confidence: 99%

Identification and Characterization of microRNAs during Retinoic Acid-Induced Regeneration of a Molluscan Central Nervous System

Walker

Spencer

Necakov

et al. 2018

Preprint

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“…VSMCs constitute the majority of the blood vessel wall (43) and their growth or programmed cell apoptosis serves an important role in the altered geometry of vessels in vascular diseases, thus promoting the rupture of aneurysms. Accordingly, VSMC apoptosis was utilized as an in vitro model of IA (35). Results from the present study demonstrated that miR-29a inhibition attenuated the apoptosis of HBVSMCs; whereas, miR-29a overexpression increased HBVSMC apoptosis.…”

Section: Discussionmentioning

confidence: 58%

“…Previous studies have demonstrated that miR-29a is able to induce cell apoptosis by activating caspase proteins (33,34). For example, miR-29a was reported to be responsible for the activation of caspase-3-induced K562 cell apoptosis (35). Therefore, miR-29a was selected for further investigation in the present study.…”

Section: Resultsmentioning

confidence: 96%

MicroRNA‑29a contributes to intracranial aneurysm by regulating the mitochondrial apoptotic pathway

Zhao

Zhang

2018

Mol Med Report

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Intracranial aneurysm (IA) is an abnormal expansion in the intracranial arteries that weakens the arterial wall by consistently pushing the vascular wall outwards, which leads to a higher risk of aneurysm rupture. A number of reports have demonstrated that apoptosis is associated with the growth and rupture of IA. MicroRNAs (miRNAs/miRs) perform vital roles in the regulation of the mitochondrial apoptotic pathway and signaling proteins. Increasing evidence has already revealed the role of miR‑29a in injury, including liver injury, cardiovascular injury and ischaemia‑reperfusion injury. However, the role of miR‑29a in IA remains unclear at present. The present study investigated the role of miR‑29a in IA pathogenesis and the underlying mechanisms. By using reverse transcription‑quantitative polymerase chain reaction and western blot analysis, the present study demonstrated that genes, including caspase‑3, ‑8 and ‑9, and proteins, including cytochrome c and myeloid cell leukemia 1 (Mcl‑1), involved in mitochondrial apoptosis pathways were upregulated in IA groups compared with controls. In addition, microarray analysis demonstrated that miR‑29a, one of the most altered miRs in IA mice, was overexpressed in IA mice compared with controls. In vitro experiments revealed that miR‑29a downregulation attenuated human brain vascular smooth muscle cell (HBVSMC) apoptosis, while miR‑29a overexpression increased the apoptosis of HBVSMCs. Furthermore, luciferase reporter analysis revealed that Mcl‑1 is a direct target gene of miR‑29a. An in vivo IA model confirmed that miR‑29a overexpression may promote apoptosis through mitochondrial pathways. It was therefore concluded that miR‑29a may contribute to the progression of IA by regulating mitochondrial apoptotic pathways. Thus, miR‑29a is a potential therapeutic target for IA.

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“…A single miRNA can take part in the different biological process by regulating the expression of its target genes (Wei et al, 2013; Wang et al, 2015; Cui et al, 2016). Based on previous studies, miR-10a was reported to be involved in collagen type I generation of hypertrophic scars, embryonic cardiac development, type 2 diabetes mellitus and chronic myeloid leukemia CD34 + cells, etc.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of MicroRNA-10a in Germ Cells Causes Male Infertility by Targeting Rad51 in Mouse and Human

et al. 2019

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Spermatogenesis is a complicated process including spermatogonial stem cells self-renewal and differentiates into mature spermatozoa. MicroRNAs (miRNAs) as a class of small non-coding RNAs play a crucial role during the process of spermatogenesis. However, the function of a plenty of miRNAs on spermatogenesis and the potential mechanisms remain largely unknown. Here, we show that genetically conditional overexpressed miR-10a in germ cells caused complete male sterility, characterized by meiotic arrested in germ cells. Analysis of miR-10a overexpression mouse testes reveals that failure of double strand break (DSB) repairs and aberrant spermatogonial differentiation. Furthermore, we identified Rad51 as a key target of miR-10a in germ cell by bioinformatics prediction and luciferase assay, which may be responsible for the infertility of the miR-10a overexpressed mice and germ cell arrested patients. Our data show that miR-10a dependent genetic regulation of meiotic process is crucial for male germ cell development and spermatogenesis in both mouse and human. These findings facilitate our understanding of the roles of miRNA-10a in spermatogenesis and male fertility.

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MiR-29 Induces K562 Cell Apoptosis by Down-Regulating FoxM1

Cited by 10 publications

References 19 publications

Identification and Characterization of microRNAs during Retinoic Acid-Induced Regeneration of a Molluscan Central Nervous System

Identification and Characterization of microRNAs during Retinoic Acid-Induced Regeneration of a Molluscan Central Nervous System

MicroRNA‑29a contributes to intracranial aneurysm by regulating the mitochondrial apoptotic pathway

Overexpression of MicroRNA-10a in Germ Cells Causes Male Infertility by Targeting Rad51 in Mouse and Human

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