| Autor: |
Guoqing Zhong, Qingping Yang, Yihua Wang, Yuan Liang, Xiaojing Wang, Dongli Zhao |
| Jazyk: |
angličtina |
| Rok vydání: |
2023 |
| Předmět: |
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| Zdroj: |
Immunity, Inflammation and Disease, Vol 11, Iss 11, Pp n/a-n/a (2023) |
| Druh dokumentu: |
article |
| ISSN: |
2050-4527 |
| DOI: |
10.1002/iid3.969 |
| Popis: |
Abstract Background What is highlighted in this study refers to the role and molecular mechanism of long noncoding RNA (lncRNA) X‐inactive specific transcript (XIST) in cells with insulin resistance (IR). Methods In this study, LX‐2 cells were applied to establish IR model in vitro. The expressions of lncRNA XIST, phosphoenolpyruvate carboxykinase (PEPCK,) and glucose‐6‐phosphatase (G6Pase) were quantified by quantitative reverse transcription polymerase chain reaction. The 2‐deoxy‐d‐glucose‐6‐phosphate (2‐DG6P) level was detected utilizing 2‐deoxy‐d‐glucose (2‐DG) uptake measurement kit. Western blot was adopted to measure the protein expressions of insulin‐like growth factor‐1 receptor (IGF‐1R), G6Pase, PEPCK, and phosphatidylinositol 3‐kinase (PI3K)/Akt pathway‐related genes. StarBase was used to predict the targeting relationship between lncRNA XIST or IGF‐1R with miR‐182‐5p, the results of which were verified by dual‐luciferase reporter, RNA pull‐down, and RNA immunoprecipitation assays. Rescue experiments were conducted to investigate the effect of miR‐182‐5p on IR cells. Next, low‐expressed lncRNA XIST and high‐expressed miR‐182‐5p were observed in IR cells. Results Upregulation of lncRNA XIST increased IGF‐1R and 2‐DG6P levels, decreased G6Pase and PEPCK expressions, and promoted PI3K/Akt pathway activation in IR cells. LncRNA XIST sponged miR‐182‐5p which targeted IGF‐1R. MiR‐182‐5p mimic reversed the above effects of lncRNA XIST overexpression on IR cells. Conclusions In conclusion, lncRNA XIST/miR‐182‐5p axis alleviates hepatic IR in vitro via IGF‐1R/PI3K/Akt signaling pathway, which could be the promising therapeutic target. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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