Wang Ye, Li Jiafu, Gao Shichun, Dang Dejing, Chen Yanlin, Li Zhiyu, Yang Hong
Internet Hospital Operation Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
First Clinical College of Medicine, Guangxi Medical University, Nanning, China.
J Endocrinol Invest. 2025 Feb;48(2):303-315. doi: 10.1007/s40618-024-02434-y. Epub 2024 Oct 1.
TMEM163 protein is a new zinc ion transporter whose regulatory role in tumors has yet to be discovered. This study aimed to analyze the expression pattern of TMEM163 in thyroid microcarcinoma and explore its potential molecular function and clinical value.
Differential analysis was performed to detect the expression pattern of TMEM163 in papillary thyroid carcinoma. Functional analysis was performed to explore the biological function of TMEM163. Logistic regression was performed to detect the relationship between TMEM163 expression and lymph node metastasis. A correlation analysis of the relationship between 163 and anoikis was performed. qRT-PCR and western blot were used to verify its expression in PTC tissues. The effect of TMEM163 on PTC cell function was studied by a series of in vitro cell experiments. The prediction model of lymph node metastasis was constructed based on the ultrasonic characteristics of PTMC and the expression of TMEM163.
The expression of TMEM163 in PTC tissue was higher than in normal thyroid tissue. In vitro, silencing TMEM163 inhibited PTC cells' proliferation, migration, and invasion, while TMEM163 overexpression exhibited the opposite effect. In addition, down-regulating its expression can inhibit the cell cycle process and induce the apoptosis of tumor cells. In pathway analysis, we demonstrated that knockout of TMEM163 significantly increased p21 expression and inhibited BCL-2 expression. Logistic regression results suggested that the expression of TMEM163 combined with PTMC ultrasound characteristics helped predict lymph node metastasis.
TMEM163 is highly expressed in PTC, which may be involved in the mechanism of anoikis, and can be used as a molecular marker to predict PTMC lymph node metastasis.
TMEM163蛋白是一种新的锌离子转运体，其在肿瘤中的调控作用尚未被发现。本研究旨在分析TMEM163在甲状腺微小癌中的表达模式，探讨其潜在的分子功能及临床价值。
进行差异分析以检测TMEM163在甲状腺乳头状癌中的表达模式。进行功能分析以探索TMEM163的生物学功能。进行逻辑回归以检测TMEM163表达与淋巴结转移之间的关系。对TMEM163与失巢凋亡之间的关系进行相关性分析。采用qRT-PCR和蛋白质免疫印迹法验证其在PTC组织中的表达。通过一系列体外细胞实验研究TMEM163对PTC细胞功能的影响。基于PTMC的超声特征和TMEM163的表达构建淋巴结转移预测模型。
TMEM163在PTC组织中的表达高于正常甲状腺组织。在体外，沉默TMEM163可抑制PTC细胞的增殖、迁移和侵袭，而TMEM163过表达则表现出相反的效果。此外，下调其表达可抑制细胞周期进程并诱导肿瘤细胞凋亡。在通路分析中，我们证明敲除TMEM163可显著增加p21表达并抑制BCL-2表达。逻辑回归结果表明，TMEM163的表达结合PTMC超声特征有助于预测淋巴结转移。
TMEM163在PTC中高表达，可能参与失巢凋亡机制，可作为预测PTMC淋巴结转移的分子标志物。
