HPV阳性头颈鳞癌侵袭性强，淋巴结转移早，可能与病毒癌基因E7的调控相关，具体机制尚不明确。前期研究发现，miRNA-106a在HPV阳性头颈鳞癌中表达较高，而RUNX3与肿瘤增殖和侵袭转移密切相关，靶基因预测RUNX3是miRNA-106a可能的靶基因。故提出科研假设：HPV16癌基因E7通过DGCR8调控miRNA-106a的表达，miRNA-106a则通过靶基因RUNX3及下游通路调控头颈鳞癌的增殖和侵袭转移。本研究从E7/miRNA-106a/RUNX3调控轴切入，以肿瘤组织、HPV阳性头颈鳞癌细胞株及其荷瘤动物作为研究对象，采用基因转染和（或）RNA干扰改变E7、DGCR8、miRNA-106a和RUNX3等的表达水平，探讨上述分子之间的调控关系及对头颈鳞癌增殖和侵袭转移的影响。本课题不仅研究调控机制，并为围绕miRNA-106a展开的靶向治疗提供依据，以期提高头颈鳞癌的预后。

HPV-positive head and neck squamous cell carcinoma (HNSCC) shows special clinical features, such as rapid proliferation, strong invasion and earlier lymph node metastasis, however, the mechanism is still unknown, which is possibly related to the regulation of virogene E7.Previsou studies found that there was a higher level expression of miRNA-106a in HPV-positive HNSCC, and RUNX3 was closely related with tumor proliferation, invasion and migration. Moreover, the miRNA targets-prediction analysis indicated that RUNX3 was a possible target-gene of miRNA-106a. As mentioned above, we speculate that E7 could regulate miRNA-106a expression by affecting DGCR8, and miRNA-106a could regulate proliferation and migration of HPV-positive HNSCC via targeting RUNX3 and downstream signaling pathway. In this research, we focus on the E7/miRNA-106a/RUNX3 regulation axis, taking HNSCC tissues, HPV-positive HNSCC cell lines, and xenografts as the study objects, we aim to explore the relationships between E7, DGCR8, miRNA-106a and RUNX3 as well as their effects on tumor proliferation and migration, through changing the expression of these molecules by gene transfection and (or) RNA inference. In summary, this research aims not only to demonstrate the regulation mechanism, but to provide evidence of target-therapy involving miRNA-106a, which is expected to improve the clinical prognosis of HNSCC.