肿瘤蛋白p53激活的lncRNA PGM5-AS1通过microRNA-1247-5p靶向R-spondin1抑制肺癌的生长和干细胞。

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2025-03-04 DOI:10.1080/13813455.2025.2459318

Peng Yang, Hong Gu, Xuanqin Wu, Geng Chen, Heng Liu, Zhongliang Chen

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引用次数: 0

摘要

目的：探讨肿瘤蛋白p53 （TP53）激活的PGM5-AS1对肺癌（LC）细胞增殖、侵袭及csc样特性的抑制作用及其机制。方法：测定PGM5-AS1对LC细胞发育的影响。干细胞标志物，细胞中的醛脱氢酶活性，以及干细胞形成球体的能力进行了测试。测定PGM5-AS1与TP53的相互作用。验证PGM5-AS1、miR-1247-5p、R-spondin1 （RSPO1）的结合链。结果：PGM5-AS1在TP53和PGM5-AS1启动子联合作用下升高。PGM5-AS1是LC细胞中miR-1247-5p的分子海绵，miR-1247-5p靶向RSPO1。升高PGM5-AS1或抑制miR-1247-5p可抑制LC细胞的生长和干性，而抑制RSPO1可逆转这一现象。结论：本研究表明，tp53升高的PGM5-AS1介导miR-1247-5p靶向RSPO1，从而抑制LC的生长和干性，代表了LC治疗的新途径。

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Tumour protein p53-activated lncRNA PGM5-AS1 suppresses lung cancer growth and stemness by targeting R-spondin1 via microRNA-1247-5p.

Objective: This study was to investigated the inhibitory role of the tumour protein p53 (TP53)-activated PGM5-AS1 in lung cancer (LC) cell proliferation, invasion, and CSC-like properties and its underlying mechanisms.

Methods: The effect of PGM5-AS1 on LC cell development was determined. Stem cell markers, aldehyde dehydrogenase activity in cells were tested, as well as the ability of stem cells to form spheroids. The interaction of PGM5-AS1 and TP53 was determined. The binding link of PGM5-AS1, miR-1247-5p, and R-spondin1 (RSPO1) was verified.

Results: PGM5-AS1 was elevated by a combination of TP53 and PGM5-AS1 promoters. PGM5-AS1 was a molecular sponge of miR-1247-5p in LC cells, and miR-1247-5p targeted RSPO1. Elevating PGM5-AS1 or repressing miR-1247-5p restrained LC cell growth and stemness, which were reversed by depression of RSPO1.

Conclusion: This study conveys that TP53-elevated PGM5-AS1 mediates miR-1247-5p to target RSPO1, thereby inhibiting LC growth and stemness, representing a novel avenue for LC therapy.

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.