目的: 探讨STC2调控HNSCC进展的作用机制。方法: HNSCC相关mRNA和miRNA通过对The Cancer Genome Atlas（TCGA）数据库分析整理获取。随后，通过MTT法、集落形成实验、流式细胞检测和迁移侵袭法，验证STC2下调后，对HNSCC细胞增殖、迁移及侵袭能力的影响。再利用生物信息学数据库，预测潜在靶向STC2的miRNA。通过qRT-PCR和荧光素酶报告基因实验，对预测获取的miR-361-3p干扰STC2的表达能力进行验证。最后，通过动物移植瘤模型验证了miR-361-3p通过下调STC2对HNSCC肿瘤发挥抑制作用。结果:STC2在HSNCC细胞中高表达。在体外，下调STC2抑制HSNCC细胞的增殖、迁移和侵袭，促进HSNCC细胞的凋亡。荧光素酶报告基因实验证实miR-361-3p可能是STC2的上游调控因子。过表达miR-361-3p下调STC2，可以抑制HNSCC细胞增殖、迁移和侵袭，促进HNSCC细胞的凋亡。结论:STC2在HNSCC细胞中呈高表达。miR-361-3p负调控STC2，进而改变HNSCC的相关细胞进展。

Objective: To investigate the upstream and downstream mechanisms of STC2 in HNSCC, and its role in cancer progression. Methods: The mRNA and miRNA expression data of HNSCC were obtained from The Cancer Genome Atlas (TCGA) databases. To detect cell proliferation, migration, and invasion ability, we used the MTT assay, colony formation experiment, flow cytometry, and migration and invasion experiment. The target mRNA of potential miRNA was predicted using bioinformatics databases, and the expression levels of target miRNA and mRNA were detected using qRT-PCR. We examined the luciferase reporter gene to verify the targeting relationship between miRNA and mRNA. To explore the relationship of STC2 and M2 macrophage, we co-cultured HNSCC and THP1 cells. Western blot was used to determine the level of signaling pathway-related proteins. Finally, we verified the promoting effects of STC2 on HNSCC cells using in vivo experiments. Results: Stanniocalcin-2 was highly expressed in HSNC cells, and promoted their proliferation, migration and invasion, and inhibited apoptosis. In addition, luciferase reporter gene assay confirmed that miR-361-3p may be an upstream regulator of STC2. The overexpression of miR-361-3p negatively regulated STC2, inhibited HNSCC cell proliferation, migration and invasion, and promoted apoptosis. Conclusion: Stanniocalcin-2 is highly expressed in HNSCC cells. miR-361-3p negatively regulates STC2, hence promoting the progression of HNSCC.

内蒙古自治区科技计划项目