下调 CLEC3B 促进肺腺癌细胞的上皮-间充质转化、迁移和侵袭。
Down-regulation of CLEC3B facilitates epithelial-mesenchymal transition, migration and invasion of lung adenocarcinoma cells.
机构信息
Department of Radiology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, China.
Department of Thoracic Surgery, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, China.
出版信息
Tissue Cell. 2022 Jun;76:101802. doi: 10.1016/j.tice.2022.101802. Epub 2022 Apr 22.
BACKGROUND
Lung adenocarcinoma (LUAD) belongs to non-small cell lung carcinoma, and the metastasis is the main cause of death in LUAD patients. It is generally accepted that cell adhesion is closely associated with tumor metastasis. Accordingly, the purpose of this study is to investigate the functions of CLEC3B to the invasion, adhesion, and migration of LUAD cells.
METHODS
Through bioinformatic analysis, CLEC3B level was found markedly down-regulated in LUAD tissue. Parallel-plate flow chamber, wound-healing and Transwell assays were taken to detect the cell adhesion, invasion, and migration. qRT-PCR and western blot analyzed expression of CLEC3B, p53 and epithelial-mesenchymal transition (EMT) marker.
RESULTS
When CLEC3B was lowly-expressed in LUAD cell lines, the cell adhesion capability was also lowered, with the EMT, migration and invasion of the cells progressed. Abnormal expression of CLEC3B was related to p53 signaling pathway.
CONCLUSION
Above all, a further investigation of the function of CLEC3B in LUAD helps us further understand the molecular mechanism of the tumor metastasis.
背景
肺腺癌（LUAD）属于非小细胞肺癌，转移是 LUAD 患者死亡的主要原因。人们普遍认为细胞黏附与肿瘤转移密切相关。因此，本研究旨在探讨 CLEC3B 对 LUAD 细胞侵袭、黏附和迁移的功能。
方法
通过生物信息学分析，发现 CLEC3B 在 LUAD 组织中明显下调。采用平行板流动室、划痕愈合和 Transwell 实验检测细胞黏附、侵袭和迁移。qRT-PCR 和 Western blot 分析 CLEC3B、p53 和上皮间质转化（EMT）标志物的表达。
结果
当 LUAD 细胞系中 CLEC3B 低表达时，细胞黏附能力也降低，细胞发生 EMT、迁移和侵袭。CLEC3B 的异常表达与 p53 信号通路有关。
结论
综上所述，进一步研究 CLEC3B 在 LUAD 中的功能有助于我们进一步了解肿瘤转移的分子机制。
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