非功能性垂体腺瘤中Claudin-9、酪氨酸激酶-2和转录信号转导和激活因子-3的表达与侵袭性的相关性。

Neuro endocrinology letters Pub Date : 2023-12-12
Abudukadier Yasen, Maimaitiyiming Tuoheti, Ba Tu, Cheng Zhang, Yu Ding, Fey Tang, Yonggang Wu
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引用次数: 0

摘要

背景:深入研究与非功能性垂体腺瘤(NFPA)侵袭性相关的病理机制是找到更好的治疗方法的当务之急。本研究初步探讨了非功能性垂体腺瘤中Claudin-9(CLDN9)、酪氨酸激酶-2(TYK2)、转录信号转导和激活因子-3(STAT3)的表达与侵袭性的相关性,以说明其病理机制:收集12例NFPA患者的临床资料和手术标本,将其分为侵袭性和非侵袭性NFPA组,每组6例。通过实时定量聚合酶链反应(qRT-PCR)、免疫印迹(WB)和免疫组化(IHC)检测两组 NFPA 组织中 CLDN9、TYK2 和 STAT3 的转录和表达水平。利用慢病毒质粒转染技术分别构建了大鼠垂体瘤GT1-1细胞系空对照组(NC)和CLDN9表达实验组(OE-CLDN9),并利用qRT-PCR检测了NC和OE-CLDN9细胞组中TYK2和STAT3的转录水平:结果:CLDN9和STAT3在浸润性NFPA组织中的表达明显高于非浸润性NFPA组织,而TYK2在浸润性NFPA组织中的表达明显低于非浸润性NFPA组织(p < 0.001);STAT3上调(p 结论:CLDN9和STAT3在浸润性NFPA组织中的表达明显高于非浸润性NFPA组织,而TYK2在浸润性NFPA组织中的表达明显低于非浸润性NFPA组织(p < 0.001):上调的CLDN9可能通过STAT3增加NFPA的侵袭性。此外,TYK2 的低表达可能会增强 NFPA 的侵袭性,这还需要进一步研究证实。这些结果可为 NFPA 的靶向治疗提供有前景的研究线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The correlation among Claudin-9, Tyrosine kinase-2, and Signal transducers and activators of transcription-3 expressions in non-functioning pituitary adenoma and invasiveness.

Background: Deeper studies on the pathological mechanism associated with invasiveness of non-functioning pituitary adenoma (NFPA) is imperative to find better treatments. This research was preliminarily conducted to investigate the correlation between the expression of Claudin-9 (CLDN9), Tyrosine kinase-2 (TYK2), Signal transducers and activators of transcription-3 (STAT3) and invasiveness in NFPA to illustrate the pathological mechanism.

Methods: Clinical data and surgical specimens of 12 patients with NFPA were collected and divided into invasive and non-invasive NFPA groups, comprising six patients for each group. CLDN9, TYK2 and STAT3 transcription and expression levels in the NFPA tissues of the two groups were detected by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting (WB) and immunohistochemistry (IHC). The lentiviral plasmid transfection technique was used to develop a rat pituitary tumour GT1-1 cell line null control group (NC) and CLDN9-overexpressed experimental group (OE-CLDN9), and TYK2 and STAT3 transcription levels in the NC and OE-CLDN9 cell groups were detected using qRT-PCR.

Results: The CLDN9 and STAT3 expressions were significantly higher in invasive than in non-invasive NFPA tissues, whereas the TYK2 expression in invasive NFPA tissues was significantly lower than that in non-invasive NFPA (p < 0.001); The STAT3 upregulated (p < 0.001) and the TYK2 downregulated (p < 0.01) after the CLDN9 overexpression.

Conclusion: Upregulated CLDN9 may increase the NFPA invasiveness through STAT3. In addition, low TYK2 expression might enhance the invasiveness in NFPA, which needs further studies to confirm. These results could provide a promising research leads for targeted treatment of NFPA.

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