MAP3K8 过表达诱导小鼠唾液腺上皮细胞鳞状细胞癌的发生。
Induction of squamous cell carcinoma after MAP3K8 overexpression in murine salivry gland epithelial cells.
机构信息
Department of Otorhinolaryngology-Head and Neck Surgery, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.
Department of Developmental Biology and Genomics, College of Veterinary Medicine, Korea Mouse Phenotyping Center, Seoul National University, Seoul, Korea.
出版信息
Head Neck. 2019 Apr;41(4):924-929. doi: 10.1002/hed.25411. Epub 2019 Feb 5.
BACKGROUND
Salivary gland neoplasms are relatively rare and comprise only 1%-4% of all human neoplasms. Salivary gland neoplasms also show an extremely wide range of morphological diversity. Currently, the genetic alterations and corresponding molecular mechanisms underlying salivary gland neoplasms development remain largely unknown.
METHOD
We generated an inducible Tet-MAP3K8::MMTV-rTA mouse model by crossing the MAP3K8 transgenic mice with MMTR-rTA transgenic mice to express MAP3K8 in the salivary gland.
RESULTS
MAP3K8 overexpression in the murine salivary glands of Tet-MAP3K8::MMTR-rTA transgenic mice induces tumorigenesis. Pathological investigations reveal partial fibrosis and adenosis of salivary glands, and foci of atypical squamoid cellular proliferation, which represent invasive squamous cell carcinoma (SCC).
CONCLUSION
MAP3K8 overexpression is associated with SCC development in murine salivary glands. It provides an in vivo framework for the understanding of molecular mechanisms underlying SCC development in the salivary glands and also for the development of a future therapeutic strategy targeting this tumor type.
背景
唾液腺肿瘤相对少见，仅占所有人类肿瘤的 1%-4%。唾液腺肿瘤在形态学上也表现出极大的多样性。目前，唾液腺肿瘤发生的遗传改变及其相应的分子机制在很大程度上仍不清楚。
方法
我们通过将 MAP3K8 转基因小鼠与 MMTR-rTA 转基因小鼠杂交，生成了一个可诱导的 Tet-MAP3K8::MMTV-rTA 小鼠模型，以在唾液腺中表达 MAP3K8。
结果
在 Tet-MAP3K8::MMTR-rTA 转基因小鼠的唾液腺中过表达 MAP3K8 可诱导肿瘤发生。病理研究显示部分唾液腺纤维化和腺病，以及不典型鳞形细胞增生灶，代表浸润性鳞状细胞癌（SCC）。
结论
MAP3K8 的过表达与小鼠唾液腺 SCC 的发生有关。它为理解唾液腺 SCC 发生的分子机制以及为针对这种肿瘤类型的未来治疗策略的发展提供了一个体内框架。
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