The novel long noncoding RNA lncRNA-Adi regulates adipogenesis.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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