喉鳞癌易侵袭转移的恶性行为导致治疗后复发及预后不良。糖酵解是肿瘤特有的代谢模式，与侵袭转移密切相关。研究表明AKT2在糖酵解助力侵袭转移中发挥重要介导作用，而PPP2R2B磷酸酶可抑制AKT激活，但上游调控机制不明。课题组通过芯片发现SKA3与AKT2在转移性喉鳞癌中上调，免疫组化表明两者共表达且与转移正相关，敲减SKA3可明显抑制喉鳞癌细胞系增殖及侵袭转移能力。文献报道SKA3与PPP2R2B相互作用，推测SKA3堆积可能阻遏PPP2R2B对下游AKT2去磷酸化；我们已证实SKA3是转移喉鳞癌独有下调分子Hsa-miR-1207-5p靶基因，同时预测到糖酵解关键分子也为其靶基因。本项目拟利用CoIP/pulldown/报告基因分析并结合体内外实验，揭示Hsa-miR-1207-5p/SKA3异常是影响糖酵解代谢重塑进而助力喉鳞癌侵袭转移的重要分子调控机制，以期为喉鳞癌生物治疗提供新靶标。

Laryngeal squamous cell carcinoma (LSCC) has the malignant behaviors of invasion and metastasis which lead to the recurrence and poor prognosis after treatment. Glycolysis, the special metabolic model in tumor, is related with invasion and metastasis. Previous studies have shown that AKT2 play an important role in tumor invasion and metastasis promoted by glycolysis. PPP2R2B could play a role in inhibition of AKT phosphorylation. However, the upstream regulatory mechanism has not been fully understood. We found that SKA3 and AKT2 were significantly upregulated in the metastatic laryngeal squamous carcinoma through genetic microarray. Immunohistochemistry showed that SKA3 and AKT2 were co-expressed and positively related to the characteristics of metastasis. Furthermore, si-SKA3 could inhibit laryngeal squamous cancer cell invasion and metastasis obviously. We conjecture that the accumulation of SKA3 could combine PPP2R2B and might inhibit dephosphorylation of AKT2 from PPP2R2B. We have confirmed SKA3 is a target gene of unique down-regulating molecular Has-miR-1207-5p in metastatic laryngeal squamous carcinoma. Meanwhile, the key molecules in glycolysis might be the target genes of Hsa-miR-1207-5p. In this study, we will illuminate the absorbingly mechanism of regulation between Hsa-miR-1207-5p/SKA3 with glycolysis and invasion by the means of CoIP, pulldown, report gene analysis in vivo and vitro respectively. Our finding would provide new targets and theoretical basis for molecular targeted therapy in LSCC.