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微小RNA-21-5p靶向磷脂酰肌醇-3激酶调节亚基1以调控核因子-κB信号通路,抑制催乳素瘤的侵袭与进展。

miR-21-5p Targets PIK3R1 to Regulate the NF-B Signaling Pathway, Inhibiting the Invasion and Progression of Prolactinoma.

作者信息

de Li Min, Yang Juan, Wu Xiao, Chen Shang Si

机构信息

Department of Rehabilitation Medicine, Affiliated Rehabilitation Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.

Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.

出版信息

Int J Endocrinol. 2025 Feb 5;2025:7741091. doi: 10.1155/ije/7741091. eCollection 2025.

Abstract

Prolactinomas (PRLs) are benign tumors with malignant characteristics that can invade the surrounding tissue structures and are challenging to treat. It has been reported that miR-21-5p expression in pituitary adenomas is correlated with tumor invasion and size. However, the mechanism of action of miR-21-5p in PRL remains unclear. Dysregulation of the phosphoinositide-3-kinase (PI3K) regulatory Subunit 1 pathway occurs frequently in cancer and plays an important role in tumor progression as an important component of the PI3K pathway. However, the role of PIK3R1 in PRL and its regulatory mechanism are unknown. In this study, we first explored the effect of miR-21-5p in PRL and then confirmed that PIK3R1 is a direct target of miR-21-5p using bioinformatics and cellular experiments. Subsequent in vitro experiments demonstrated that overexpression of PIK3R1 significantly attenuated the biological effects of miR-21-5p in PRL cells, such as promoting proliferation and invasion. Finally, we explored the mechanism by which PIK3R1 affects PRL progression and found that the inhibition of IBa degradation by PIK3R1 impacts PRL progression via the miR-21-5p/PIK3R1/MMP pathway.

摘要

催乳素瘤(PRL)是具有恶性特征的良性肿瘤,可侵犯周围组织结构,治疗具有挑战性。据报道,垂体腺瘤中miR-21-5p的表达与肿瘤侵袭和大小相关。然而,miR-21-5p在PRL中的作用机制仍不清楚。磷酸肌醇-3-激酶(PI3K)调节亚基1途径的失调在癌症中频繁发生,并作为PI3K途径的重要组成部分在肿瘤进展中起重要作用。然而,PIK3R1在PRL中的作用及其调节机制尚不清楚。在本研究中,我们首先探讨了miR-21-5p在PRL中的作用,然后通过生物信息学和细胞实验证实PIK3R1是miR-21-5p的直接靶点。随后的体外实验表明,PIK3R1的过表达显著减弱了miR-21-5p在PRL细胞中的生物学效应,如促进增殖和侵袭。最后,我们探讨了PIK3R1影响PRL进展的机制,发现PIK3R1对IκB降解的抑制通过miR-21-5p/PIK3R1/MMP途径影响PRL进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/11824381/8209a6ff6467/IJE2025-7741091.001.jpg

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