Transient receptor potential melastatin (TRPM) 通道与细胞增殖和细胞存活有关。TRPM 亚家族有八个成员（TRPM1-8）。本研究旨在研究 TRPM6 在人类口腔癌发生中的表达。66 个口腔鳞状细胞癌 (OSCC)、47 个具有中-重度上皮异形 (ED) 的口腔潜在恶性疾病 (OPMD)、28 个具有轻度 ED 的 OPMD，以及 33 个正常口腔黏膜 (NOM) 样本进行免疫组织化学染色。使用两个人类口腔癌细胞系 (OCCLs)、一种口腔癌前细胞系 (DOK) 和一种正常口腔角质细胞培养 (HOK) 进行 Western blot 分析。用 TRPM6 小干扰 RNA 转染的 OCCLs 进行增殖、迁移、侵袭试验和胞内钙离子浓度评估。与正常样本相比，OSCC 中TRPM6 蛋白表达显著增加。OCCLs 中 TRPM6 蛋白表达显著高于 HOK。与未转染的 OCCL 相比，经TRPM6 siRNA 转染的 OCCLs 的增殖、迁移、侵袭和胞内钙离子浓度显著降低。中-重度 ED 的 OPMD 中 TRPM6 蛋白水平显著增加，与轻度 ED 的OPMD 相比差异显著。我们的结果表明 TRPM6 过度表达可能与人类口腔癌发生有关。© 2022 中华牙科学会。由 Elsevier B.V. 提供出版服务。

Transient receptor potential melastatin (TRPM) channel is involved in cell proliferation and cell survival. Eight members (TRPM1-8) are within the TRPM subfamily. The current study is aimed to investigate TRPM6 expression in human oral carcinogenesis.Sixty-six oral squamous cell carcinomas (OSCCs), 47 oral potentially malignant disorders (OPMD) with moderate-severe epithelial dysplasia (ED), 28 OPMD with mild ED, and 33 normal oral mucosa (NOM) samples were subjected to immunohistochemical staining. Two human oral cancer cell lines (OCCLs), an oral premalignant cell line (DOK), and a normal oral keratinocyte culture (HOK) were used for Western blot analysis. OCCLs were evaluated for proliferation, migration, invasion assays, and intracellular calcium concentration.TRPM6 protein expression in OSCC was significantly increased as compared with normal samples. Protein expression of TRPM6 in OCCLs was significantly higher as compared with HOK. Significant decreases in degrees of proliferation, migration, invasion, and intracellular calcium concentration were noted in OCCLs with TRPM6 siRNA transfection as compared with those without transfection. Significantly increased TRPM6 protein level was noted in OPMD with moderate-severe ED as compared with those with mild ED.Our results implicate that TRPM6 overexpression is potentially related to human oral carcinogenesis.© 2022 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V.