Wu Yanhui, Zhang Shunchu, Zou Guimei
Department of Stomatology, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China.
Department of Stomatology, Jiangsu Cancer Hospital, Nanjing, Jiangsu Province, China.
Cytojournal. 2025 Jan 22;22:5. doi: 10.25259/Cytojournal_132_2024. eCollection 2025.
Transmembrane Emp24 Domain Containing 2 TMED2) is a mediator of membrane protein trafficking involved in intracellular protein transport. Recent research suggests that TMED2 plays an important role in the development and metastasis of tumors; however, its exact mechanisms in oral cancer (OC) remain unclear. This study aims to elucidate the role and possible mechanisms of TMED2 in OC.
We investigated the impact of TMED2 knockdown on the invasion, migration, and proliferation capabilities of OC cells. Furthermore, we analyzed the and interactions between TMED2 and polypeptide-N-acetylgalactosaminyltransferase 7 (GALNT7) as well as explored the regulatory function of TMED2 on GALNT7. The alterations in stem cell markers were assessed using clone formation assays, western blot, and quantitative real-time polymerase chain reaction.
The upregulation of TMED2 promoted the proliferation and invasion abilities of OC cells. Further analysis revealed that TMED2 enhanced the stem-like properties and tumorigenicity of OC cells by directly regulating the expression of GALNT7. and results suggested that silencing TMED2 expression reduced the incidence of OC.
Our data imply that TMED2 stimulates GALNT7 transcription, which in turn amplifies the stem-like characteristics and carcinogenic potential of OC cells. Moreover, the block of TMED2 prevents cancers from growing and spreading . This finding provides a new therapeutic target for the treatment of OC and highlights the critical role of TMED2 in the condition.
跨膜含Emp24结构域蛋白2(TMED2)是参与细胞内蛋白质运输的膜蛋白转运介质。最近的研究表明,TMED2在肿瘤的发生发展和转移中起重要作用;然而,其在口腔癌(OC)中的具体机制仍不清楚。本研究旨在阐明TMED2在OC中的作用及可能机制。
我们研究了敲低TMED2对OC细胞侵袭、迁移和增殖能力的影响。此外,我们分析了TMED2与多肽-N-乙酰半乳糖胺基转移酶7(GALNT7)之间的相互作用,并探讨了TMED2对GALNT7的调控功能。使用克隆形成试验、蛋白质免疫印迹法和定量实时聚合酶链反应评估干细胞标志物的变化。
TMED2的上调促进了OC细胞的增殖和侵袭能力。进一步分析表明,TMED2通过直接调节GALNT7的表达增强了OC细胞的干细胞样特性和致瘤性。结果表明,沉默TMED2表达可降低OC的发生率。
我们的数据表明,TMED2刺激GALNT7转录,进而放大OC细胞的干细胞样特征和致癌潜力。此外,阻断TMED2可防止癌症生长和扩散。这一发现为OC的治疗提供了新的治疗靶点,并突出了TMED2在该疾病中的关键作用。