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肢端肥大症中的 microRNA:在发病机制和第一代生长抑素受体配体反应中的作用。

MicroRNA in Acromegaly: Involvement in the Pathogenesis and in the Response to First-Generation Somatostatin Receptor Ligands.

机构信息

Neuroendocrinology Research Center, Endocrinology Division, Medical School and Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-901, Brazil.

Neuropathology and Molecular Genetics Laboratory, Instituto Estadual do Cérebro Paulo Niemeyer, Rio de Janeiro 20231-092, Brazil.

出版信息

Int J Mol Sci. 2022 Aug 4;23(15):8653. doi: 10.3390/ijms23158653.

DOI:10.3390/ijms23158653
PMID:35955787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9368811/
Abstract

Acromegaly is a chronic and systemic disease due to excessive growth hormone and insulin-like growth factor type I caused, in the vast majority of cases, by a GH-secreting pituitary adenoma. About 40% of these tumors have somatic mutations in the stimulatory G protein alpha-subunit 1 gene. The pathogenesis of the remaining tumors, however, is still not fully comprehended. Surgery is the first-line therapy for these tumors, and first-generation somatostatin receptor ligands (fg-SRL) are the most prescribed medications in patients who are not cured by surgery. MicroRNAs are small, non-coding RNAs that control the translation of many mRNAs, and are involved in the post-transcriptional regulation of gene expression. Differentially expressed miRNAs can explain differences in the pathogenesis of acromegaly and tumor resistance. In this review, we focus on the most validated miRNAs, which are mainly involved in acromegaly’s tumorigenesis and fg-SRL resistance, as well as in circulating miRNAs in acromegaly.

摘要

肢端肥大症是一种由生长激素和胰岛素样生长因子 I 过度分泌引起的慢性系统性疾病,在绝大多数情况下是由生长激素分泌垂体腺瘤引起的。这些肿瘤中约有 40%存在刺激 G 蛋白α亚单位 1 基因的体细胞突变。然而,其余肿瘤的发病机制仍未完全理解。手术是这些肿瘤的一线治疗方法,第一代生长抑素受体配体(fg-SRL)是手术后未治愈患者最常开的药物。微小 RNA 是一种小的非编码 RNA,可以控制许多 mRNA 的翻译,并参与基因表达的转录后调控。差异表达的 miRNA 可以解释肢端肥大症和肿瘤耐药性发病机制的差异。在这篇综述中,我们主要关注那些经过最充分验证的 miRNA,它们主要与肢端肥大症的肿瘤发生和 fg-SRL 耐药性以及肢端肥大症的循环 miRNA 有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93b5/9368811/9eead8e3e608/ijms-23-08653-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93b5/9368811/600c61f598df/ijms-23-08653-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93b5/9368811/af9111b2b781/ijms-23-08653-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93b5/9368811/9eead8e3e608/ijms-23-08653-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93b5/9368811/600c61f598df/ijms-23-08653-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93b5/9368811/af9111b2b781/ijms-23-08653-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93b5/9368811/9eead8e3e608/ijms-23-08653-g003.jpg

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The biochemical and clinical implications of phosphatase and tensin homolog deleted on chromosome ten in different cancers.
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Cancers (Basel). 2021 Sep 28;13(19):4857. doi: 10.3390/cancers13194857.
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