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长链非编码RNA OIP5-AS1作为一种竞争性内源RNA,通过吸附miR-217促进谷氨酰胺分解代谢和恶性黑色素瘤生长。

Long noncoding RNA OIP5-AS1 acts as a competing endogenous RNA to promote glutamine catabolism and malignant melanoma growth by sponging miR-217.

作者信息

Luan Wenkang, Zhang Xuanfeng, Ruan Hongru, Wang Jinlong, Bu Xuefeng

机构信息

Department of Plastic Surgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, China.

Department of General Surgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, China.

出版信息

J Cell Physiol. 2019 Sep;234(9):16609-16618. doi: 10.1002/jcp.28335. Epub 2019 Feb 18.

DOI:10.1002/jcp.28335
PMID:30779126
Abstract

The long noncoding RNA (lncRNA) OIP5-AS1 has been considered to promote the growth and metastasis of many human tumors. However, the role of OIP5-AS1 in melanoma has not been reported. In this study, we found that OIP5-AS1 levels were significantly elevated in melanoma tissue and that high OIP5-AS1 expression was an independent risk factor for the poor survival of patients with melanoma. miR-217 suppressed glutamine catabolism in melanoma cells by targeting glutaminase (GLS), the rate-limiting enzyme of glutamine catabolism. We also demonstrated that OIP5-AS1 acted as a sponge of miR-217 to upregulate GLS expression, thus promoting glutamine catabolism and melanoma growth. Overall, this result elucidates a new mechanism for OIP5-AS1 in metabolism in melanoma and provides a potential therapeutic target for patients with melanoma.

摘要

长链非编码RNA(lncRNA)OIP5-AS1被认为可促进多种人类肿瘤的生长和转移。然而,OIP5-AS1在黑色素瘤中的作用尚未见报道。在本研究中,我们发现黑色素瘤组织中OIP5-AS1水平显著升高,且OIP5-AS1高表达是黑色素瘤患者生存不良的独立危险因素。miR-217通过靶向谷氨酰胺分解代谢的限速酶谷氨酰胺酶(GLS)来抑制黑色素瘤细胞中的谷氨酰胺分解代谢。我们还证明,OIP5-AS1作为miR-217的海绵,上调GLS表达,从而促进谷氨酰胺分解代谢和黑色素瘤生长。总体而言,该结果阐明了OIP5-AS1在黑色素瘤代谢中的新机制,并为黑色素瘤患者提供了潜在的治疗靶点。

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引用本文的文献

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Glutamine Metabolism: Molecular Regulation, Biological Functions, and Diseases.谷氨酰胺代谢:分子调控、生物学功能与疾病
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2
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Transl Cancer Res. 2024 Jun 30;13(6):3046-3061. doi: 10.21037/tcr-24-630. Epub 2024 Jun 27.
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A metabolic perspective on nitric oxide function in melanoma.
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Front Cell Dev Biol. 2023 Jun 13;11:1164301. doi: 10.3389/fcell.2023.1164301. eCollection 2023.
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Amino acid metabolism regulated by lncRNAs: the propellant behind cancer metabolic reprogramming.lncRNAs 调控的氨基酸代谢:癌症代谢重编程的推进剂。
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