TGFBR3 inhibits progression of papillary thyroid cancer by inhibiting the PI3K/AKT pathway and EMT.

IF 2.6 3区医学 Q3 ENDOCRINOLOGY & METABOLISM

Endocrine Connections Pub Date : 2024-11-21 Print Date: 2024-12-01 DOI:10.1530/EC-24-0270

Hanrong Zhang, Junxin Chen, Xin Chen, Chuimian Zeng, Pengyuan Zhang, Jiewen Jin, Haipeng Xiao, Yanbing Li, Hongyu Guan, Hai Li

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引用次数: 0

Abstract

Background: Transforming growth factor beta receptor III (TGFBR3) has been shown to play a tumor-suppressive role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains unknown.

Method: TGFBR3 expression levels in PTC were analyzed utilizing The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Edu, wound healing, and Transwell assays were used to evaluate cell proliferation, migration, and invasion. Transcriptome sequencing, quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR), and Western blotting were used to detect the underlying mechanism of TGFBR3 in PTC progression.

Result: This study demonstrated that TGFBR3 expression was significantly down-regulated in PTC compared to normal thyroid tissues. Low expression of TGFBR3 was associated with poor prognosis of patients with PTC. Furthermore, TGFBR3 expression positively correlated with thyroid differentiation score. In investigating the biological impact of TGFBR3 overexpression in PTC cell lines, we found that the proliferation, migration, and invasion of PTC cells were significantly inhibited in response to TGFBR3 overexpression. Moreover, we also demonstrated that overexpression of TGFBR3 inhibited the PI3K/AKT pathway and epithelial-mesenchymal transformation processes. Lastly, TGFBR3 expression was found to be involved in tumor immune infiltration, highlighting its potential influence on immune dynamics within the tumor microenvironment in PTC.

Conclusion: TGFBR3 plays a tumor-suppressive role in PTC progression by inhibiting the PI3K/AKT pathway and epithelial mesenchymal transformation.

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TGFBR3通过抑制PI3K/AKT通路和EMT来抑制甲状腺乳头状癌的进展。

背景：转化生长因子β受体III（TGFBR3）已被证明在多种癌症中发挥抑制肿瘤的作用。然而，它在甲状腺乳头状癌（PTC）中的作用仍然未知：方法：利用TCGA和GEO数据库分析TGFBR3在PTC中的表达水平。方法：利用 TCGA 和 GEO 数据库分析 TGFBR3 在 PTC 中的表达水平。通过转录组测序、qRT-PCR和Western印迹检测TGFBR3在PTC进展中的潜在机制：结果：研究表明，与正常甲状腺组织相比，TGFBR3在PTC中的表达明显下调。TGFBR3的低表达与PTC患者的不良预后有关。此外，TGFBR3的表达与甲状腺分化评分呈正相关。在研究 TGFBR3 在 PTC 细胞系中过度表达的生物学影响时，我们发现 TGFBR3 过度表达会显著抑制 PTC 细胞的增殖、迁移和侵袭。此外，我们还发现过表达 TGFBR3 可抑制 PI3K/AKT 通路和上皮间质转化过程。最后，我们发现TGFBR3的表达参与了肿瘤免疫浸润，这凸显了它对PTC肿瘤微环境中免疫动态的潜在影响：结论：TGFBR3通过抑制PI3K/AKT通路和EMT在PTC进展过程中发挥抑瘤作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Endocrine Connections Medicine-Internal Medicine

CiteScore

5.00

自引率

3.40%

发文量

361

审稿时长

6 weeks

期刊介绍： Endocrine Connections publishes original quality research and reviews in all areas of endocrinology, including papers that deal with non-classical tissues as source or targets of hormones and endocrine papers that have relevance to endocrine-related and intersecting disciplines and the wider biomedical community.