Obesity is considered as a high‐risk susceptibility state for most metabolic disorders and is directly related to preadipocyte differentiation or adipogenesis. Long noncoding RNAs (lncRNAs) are the key factors which have regulatory functions on various critical physiological and biological processes. PVT1 was identified as an oncogenic lncRNA which could promote angiogenesis in gastric cancer. However, the functions and molecular pathways related to PVT1 in adipogenesis had not been clarified yet. In the current study, the purpose was to identify the effects of lncRNA PVT1 on adipogenesis and the relevant molecular processes. Quantitative real‐time polymerase chain reaction (RT‐qPCR) was used to quantify PVT1 expression. The mechanism for PVT1 to participate in 3T3‐L1 adipogenesis was identified by lentivirus‐mediated gain‐ and loss‐of‐function tests. The potential association of PVT1 with cell viability was checked by CCK‐8 assay and EdU staining. The gene expression for cytokines was determined by quantitative PCR (qPCR) and western blotting. PVT1 expression level was strongly upregulated after 3T3‐L1 preadipocytes differentiated. In mice, PVT1 was abundantly expressed in adipose tissue, and the obese mice had higher PVT1 expression in adipose tissue than that of nonobese mice. Predominantly, PVT1 was found inside the nuclei. Overexpressed PVT1 could promote 3T3‐L1 adipocyte differentiation as proved, which was the cause for the ability to accelerate lipid accumulation, by upregulating the expression of peroxisome proliferator activated receptor gamma, CCAAT/enhancer‐binding protein α, and adipocyte protein 2, while knockdown of PVT1 caused opposite effects. The RNA immunoprecipitation demonstrated the binding relationship between PVT1 and STAT3 suggesting the potential role of STAT3 in 3T3‐L1 preadipocyte differentiation. Furthermore, PVT1 could promote fatty acid synthesis but inhibit fatty acid oxidation. PVT1 was positively associated with 3T3‐L1 preadipocyte differentiation, which highlighted the potential of PVT1 as a therapeutic target for obesity treatment.

中文翻译：

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长链非编码 RNA PVT1 在调节 3T3-L1 前脂肪细胞增殖和分化中的作用和可能机制

肥胖被认为是大多数代谢紊乱的高危易感状态，并且与前脂肪细胞分化或脂肪生成直接相关。长链非编码 RNA (lncRNA) 是对各种关键生理和生物过程具有调节功能的关键因素。PVT1被鉴定为致癌lncRNA，可以促进胃癌血管生成。然而，PVT1在脂肪生成中的功能和分子通路尚未阐明。在目前的研究中，目的是确定 lncRNA PVT1 对脂肪生成和相关分子过程的影响。定量实时聚合酶链反应 (RT-qPCR) 用于量化 PVT1 表达。PVT1 参与 3T3-L1 脂肪生成的机制是通过慢病毒介导的功能获得和功能丧失测试确定的。通过 CCK-8 测定和 EdU 染色检查 PVT1 与细胞活力的潜在关联。通过定量 PCR (qPCR) 和蛋白质印迹确定细胞因子的基因表达。3T3-L1前脂肪细胞分化后，PVT1表达水平强烈上调。在小鼠中，PVT1 在脂肪组织中大量表达，肥胖小鼠在脂肪组织中的 PVT1 表达高于非肥胖小鼠。主要是在细胞核内发现了 PVT1。过表达的 PVT1 可以促进 3T3-L1 脂肪细胞分化，这是通过上调过氧化物酶体增殖物激活受体 γ 的表达加速脂质积累能力的原因，CCAAT/增强子结合蛋白 α 和脂肪细胞蛋白 2，而 PVT1 的敲低会导致相反的效果。RNA 免疫沉淀证明了 PVT1 和 STAT3 之间的结合关系，表明 STAT3 在 3T3-L1 前脂肪细胞分化中的潜在作用。此外，PVT1可以促进脂肪酸合成但抑制脂肪酸氧化。PVT1 与 3T3-L1 前脂肪细胞分化呈正相关，这突出了 PVT1 作为肥胖治疗靶点的潜力。PVT1可以促进脂肪酸合成但抑制脂肪酸氧化。PVT1 与 3T3-L1 前脂肪细胞分化呈正相关，这突出了 PVT1 作为肥胖治疗靶点的潜力。PVT1可以促进脂肪酸合成但抑制脂肪酸氧化。PVT1 与 3T3-L1 前脂肪细胞分化呈正相关，这突出了 PVT1 作为肥胖治疗靶点的潜力。