Thyroid cancer is the most common type of endocrine cancer. Chemokine-like factor (CKLF)-like MARVEL transmembrane domain containing 6 (CMTM6) is recognized as one of its potential immunotherapy targets. The purpose of this study was to investigate the role and molecular mechanism of CMTM6 in regulating the development of thyroid cancer cells. In this study, expression levels of CMTM6 and the sodium/iodide symporter (NIS) were detected by qRT-PCR. Additionally, colony formation assay and flow cytometry were used to detect cell proliferation and apoptosis, while expression levels of various proteins were assessed using Western blotting. Further, the apoptosis and invasion capacity of cells were investigated by scratch and transwell experiments. Finally, the effect of CMTM6 on the epithelial-mesenchymal transition (EMT) of thyroid cancer cells was determined by immunofluorescence assay, which measured the expression levels of epithelial and mesenchymal phenotypic markers. The results of qRT-PCR experiments showed that CMTM6 was highly expressed in thyroid cancer tissues and cells. In addition, knockdown of CMTM6 expression significantly increased NIS expression. Function experiments demonstrated that small interfering (si)-CMTM6 treatment inhibited the proliferation, migration, invasion, and EMT of thyroid cancer cells, while promoting apoptosis of FTC133 cells. Furthermore, mechanistic studies showed that mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) phosphorylation were inhibited by si-CMTM6, as demonstrated by Western blot experiments. In conclusion, our findings demonstrated the role of CMTM6 in the metastasis of thyroid cancer. Briefly, CMTM6 exerts its tumor-promoting effect through the MAPK signaling pathway and could potentially be used as a valuable biomarker for thyroid cancer diagnosis and prognosis.

甲状腺癌是最常见的内分泌癌类型。趋化因子样因子（CKLF）样MARVEL跨膜结构域含有6（CMTM6）被认为是其潜在的免疫治疗靶点之一。本研究的目的是探讨CMTM6在调节甲状腺癌细胞发生发展中的作用及分子机制。在本研究中，通过 qRT-PCR 检测了 CMTM6 和钠/碘同向转运蛋白 (NIS) 的表达水平。此外，使用集落形成测定和流式细胞术检测细胞增殖和凋亡，同时使用蛋白质印迹评估各种蛋白质的表达水平。进一步通过划痕实验和Transwell实验研究细胞的凋亡和侵袭能力。最后，通过免疫荧光法测定上皮和间质表型标志物的表达水平，确定CMTM6对甲状腺癌细胞上皮-间质转化（EMT）的影响。qRT-PCR实验结果表明，CMTM6在甲状腺癌组织和细胞中高表达。此外，CMTM6表达的敲低显着增加了NIS表达。功能实验表明，小干扰(si)-CMTM6处理可抑制甲状腺癌细胞的增殖、迁移、侵袭和EMT，同时促进FTC133细胞凋亡。此外，机制研究表明，蛋白质印迹实验证明，丝裂原激活蛋白激酶 (MAPK) 和细胞外信号调节激酶 (ERK) 磷酸化受到 si-CMTM6 的抑制。总之，我们的研究结果证明了 CMTM6 在甲状腺癌转移中的作用。简而言之，CMTM6通过MAPK信号通路发挥其促肿瘤作用，并有可能作为甲状腺癌诊断和预后的有价值的生物标志物。