目的 探究长链非编码RNA（LncRNA）小核仁RNA宿主基因（SNHG）22调控微小RNA（miR）-27b-3p对口腔鳞状细胞癌（OSCC）细胞增殖、侵袭和迁移的影响。 方法 收集52例OSCC患者的癌组织及癌旁组织标本，体外培养人正常口腔角质细胞HOK和3种人OSCC细胞（CAL-27、SCC-25和HSC-3），实时荧光定量聚合酶链反应（qRT-PCR）检测癌组织、癌旁组织、HOK细胞和3种OSCC细胞中SNHG22、miR-27b-3p表达情况。对SCC-25细胞进行转染并将其分为Ctrl组（未进行转染）、si-SNHG22组、si-NC组、miR-27b-3p inhibitor组、inhibitor-NC组、si-SNHG22+inhibitor-NC组和si-SNHG22+miR-27b-3p inhibitor组，检测各组SCC-25细胞增殖情况［细胞计数试剂盒8（CCK-8）法检测增殖率、流式细胞术检测增殖指数（PI）］；Transwell实验检测各组SCC-25细胞侵袭情况；划痕愈合实验检测各组SCC-25细胞迁移情况；双荧光素酶实验验证SNHG22与miR-27b-3p的靶向作用关系。 结果 与癌旁组织比较，OSCC癌组织中SNHG22表达显著升高，miR-27b-3p表达显著降低（P<0.05）；与HOK细胞比较，CAL-27、SCC-25和HSC-3细胞中SNHG22表达显著升高，miR-27b-3p表达显著降低，且SCC-25细胞中SNHG22与miR-27b-3p的表达与HOK细胞差异最大（P<0.05）。与Ctrl组比较，si-SNHG22组SCC-25细胞增殖率、PI、侵袭数和划痕面积愈合率均显著减少（P<0.05），miR-27b-3p inhibitor组SCC-25细胞增殖率、PI、侵袭数和划痕面积愈合率均显著增加（P<0.05）；与si-SNHG22组比较，si-SNHG22+miR-27b-3p inhibi-tor组SCC-25细胞增殖率、PI、侵袭数和划痕面积愈合率均显著增加（P<0.05）。双荧光素酶实验显示SNHG22与miR-27b-3p存在靶向作用关系。 结论 SNHG22在OSSC中高表达，miR-27b-3p在OSSC中低表达，SNHG22可能通过海绵化miR-27b-3p促进SCC-25细胞增殖、侵袭和迁移，SNHG22/miR-27b-3p轴可能是OSCC一个新的诊断和治疗靶点。

Objective This study aimed to investigate the influences of long noncoding RNA small nucleolar RNA host gene (SNHG) 22 on the proliferation, invasion, and migration of oral squamous cell carcinoma (OSCC) cells by regulating microRNA (miR)-27b-3p. Methods Cancer tissue and paracancerous tissue specimens of 52 OSCC patients were collected. Human normal oral keratinocytes (HOK) and three kinds of human OSCC cells (CAL-27, SCC-25, and HSC-3) were cultured in vitro. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of SNHG22 and miR-27b-3p in cancer tissues, adjacent tissues, HOK cells, and three kinds of OSCC cells. SCC-25 cells were transfected and separated into the following groups: control (no transfection), si-SNHG22, si-NC, miR-27b-3p inhibitor, inhibitor-NC, si-SNHG22+inhibitor-NC, and si-SNHG22+miR-27b-3p inhibitor. The proliferation of SCC-25 cells in each group was detected by cell-counting kit 8 method, and proliferation index (PI) was detected by flow cytometry. Transwell assay was applied to detect the invasion of SCC-25 cells in each group. Scratch-area healing experiment was applied to detect the migration of SCC-25 cells in each group. Dual-luciferase experiment was applied to verify the targeting relationship between SNHG22 and miR-27b-3p. Results Compared with adjacent tissues, SNHG22 expression in OSCC cancer tissues significantly increased, and the expression of miR-27b-3p significantly decreased (P<0.05). Compared with HOK cells, SNHG22 expression significantly increased in CAL-27 cells, SCC-25 cells, and HSC-3 cells, and the expression of miR-27b-3p significantly decreased. The expression in SCC-25 cells differed the most from that in HOK cells (P<0.05). Compared with the control group, the SCC-25 cell-proliferation rate, PI, invasion number, and scratch-area healing rate in the si-SNHG22 group decreased significantly (P<0.05). The SCC-25 cell-proliferation rate, PI, invasion number, and scratch-area healing rate in the miR-27b-3p inhibitor group increased significantly (P<0.05); compared with the si-SNHG22 group. The SCC-25 cell-proliferation rate, PI, invasion number, and scratch-area healing rate in the si-SNHG22+miR-27b-3p inhibitor group increased significantly (P<0.05). Dual-luciferase experiments showed that SNHG22 had a targeting relationship with miR-27b-3p. Conclusion SNHG22 was highly expressed in OSSC, whereas miR-27b-3p was lowly expressed. SNHG22 may promote the proliferation, invasion, and migration of SCC-25 cells through sponge miR-27b-3p. The SNHG22/miR-27b-3p axis may be a new diagnostic and therapeutic target for OSCC.