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The novel long noncoding RNA lncRNA-Adi regulates adipogenesis.
STEM CELLS Translational Medicine ( IF 5.4 ) Pub Date : 2020-05-01 , DOI: 10.1002/sctm.19-0438 Yuanwei Chen 1, 2 , Kaide Li 1 , Xiao Zhang 1 , Jinlong Chen 1 , Meisheng Li 1 , Lei Liu 1
STEM CELLS Translational Medicine ( IF 5.4 ) Pub Date : 2020-05-01 , DOI: 10.1002/sctm.19-0438 Yuanwei Chen 1, 2 , Kaide Li 1 , Xiao Zhang 1 , Jinlong Chen 1 , Meisheng Li 1 , Lei Liu 1
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Adipogenesis participates in many physiological and pathological processes, such as obesity and diabetes, and is regulated by a series of precise molecular events. However, the molecules involved in this regulation have not been fully characterized. In this study, we identified a long noncoding (lnc)RNA, lncRNA‐Adi, which is highly expressed in adipose tissue‐derived stromal cells (ADSCs) that are differentiating into adipocytes. Knockdown of lncRNA‐Adi impaired the adipogenic differentiation ability of ADSCs. Moreover, lncRNA‐Adi was found to interact with microRNA (miR)‐449a to enhance the expression of cyclin‐dependent kinase (CDK)6 during adipogenesis. The mechanism by which lncRNA‐Adi regulates adipogenesis was determined to involve an lncRNA‐Adi‐miR‐449a interaction that competes with the CDK6 3′ untranslated region to increase CDK6 translation and activate the pRb‐E2F1 pathway to promote adipogenesis. These findings provide valuable information and a new study angle to search for therapeutic targets against metabolic disorders such as obesity and diabetes.
中文翻译：
新的长非编码RNA lncRNA-Adi调节脂肪形成。
脂肪形成参与许多生理和病理过程，例如肥胖和糖尿病，并受一系列精确的分子事件调节。但是，尚未完全表征参与该调控的分子。在这项研究中，我们鉴定了一个长的非编码（lnc）RNA，即lncRNA-Adi，该基因在分化为脂肪细胞的脂肪组织来源的基质细胞（ADSC）中高表达。抑制lncRNA-Adi损害了ADSCs的成脂分化能力。此外，还发现lncRNA-Adi可与microRNA（miR）-449a相互作用，从而在脂肪形成过程中增强细胞周期蛋白依赖性激酶（CDK）6的表达。确定了lncRNA-Adi调节脂肪形成的机制涉及lncRNA-Adi-miR-449a相互作用，该相互作用与CDK6 3'非翻译区竞争，从而增加CDK6的翻译并激活pRb-E2F1途径来促进脂肪形成。这些发现为寻找针对肥胖症和糖尿病等代谢性疾病的治疗靶标提供了有价值的信息和新的研究视角。
更新日期：2020-05-01
中文翻译：
新的长非编码RNA lncRNA-Adi调节脂肪形成。
脂肪形成参与许多生理和病理过程，例如肥胖和糖尿病，并受一系列精确的分子事件调节。但是，尚未完全表征参与该调控的分子。在这项研究中，我们鉴定了一个长的非编码（lnc）RNA，即lncRNA-Adi，该基因在分化为脂肪细胞的脂肪组织来源的基质细胞（ADSC）中高表达。抑制lncRNA-Adi损害了ADSCs的成脂分化能力。此外，还发现lncRNA-Adi可与microRNA（miR）-449a相互作用，从而在脂肪形成过程中增强细胞周期蛋白依赖性激酶（CDK）6的表达。确定了lncRNA-Adi调节脂肪形成的机制涉及lncRNA-Adi-miR-449a相互作用，该相互作用与CDK6 3'非翻译区竞争，从而增加CDK6的翻译并激活pRb-E2F1途径来促进脂肪形成。这些发现为寻找针对肥胖症和糖尿病等代谢性疾病的治疗靶标提供了有价值的信息和新的研究视角。
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