目的 分析LncRNA SNHG16靶向调控miR-516a-5p对结直肠癌细胞增殖、侵袭和迁移能力的影响。 方法 采用实时荧光RT-PCR检测lncRNA SNHG16、miR-516a-5p表达，构建抑制lncRNA SNHG16表达的SW480细胞，并对SW480细胞转染，分为NC组、si-NC组、si-SNHG16组、miR-NC组、miR-516a-5p组、si-SNHG16+anti-miR-NC组、si-SNHG16+anti-miR-516a-5p组，检测各组细胞增殖、凋亡侵袭、迁移情况。 结果 与癌旁组织相比，结直肠癌组织中lncRNA SNHG16表达水平升高，miR-516a-5p表达水平降低（P < 0.05）。与FHC组相比，HCT116组、SW620组、SW480组细胞中lncRNA SNHG16表达水平升高，miR-516a-5p表达水平较低，且SW480组lncRNA SNHG16水平最高、miR-516a-5p水平最低（P < 0.05）。与si-NC组相比，si-SNHG16组lncRNA SNHG16表达水平降低（P < 0.05），表明干扰lncRNA SNHG16表达的SW480细胞株构建成功，与si-NC组相比，si-SNHG16组CyclinD1、MMP-2、MMP-9、OD值、迁移细胞数、侵袭细胞数降低，凋亡细胞升高（P < 0.05）。与miR-NC组相比，miR-516a-5p组miR-516a-5p表达水平升高（P < 0.05），表明高表达miR-516a-5p的SW480细胞株构建成功，与miR-NC组相比，miR-516a-5p组CyclinD1、MMP-2、MMP-9、OD值、迁移细胞数、侵袭细胞数降低，凋亡细胞升高（P < 0.05）。双荧光素酶报告试验显示，与miR-NC组相比，miR-516a-5p可使SNHG16荧光素酶活性降低（P < 0.05），对MUT-SNHG16荧光素酶活性影响较小（P > 0.05）。与si-NC组相比，抑制lncRNA SNHG16表达可使SW480细胞中miR-516a-5p表达、凋亡细胞升高，CyclinD1、MMP-2、MMP-9、OD值、迁移细胞数、侵袭细胞数降低（P < 0.05），与si-SNHG16+anti-miR-NC组相比，si-SNHG16+anti-miR-516a-5p组miR-516a-5p表达、凋亡细胞降低，CyclinD1、MMP-2、MMP-9、OD值、迁移细胞数、侵袭细胞数升高（P < 0.05）。 结论 干扰lncRNA SNHG16表达，可对miR-516a-5p表达进行调控，抑制结直肠癌细胞增殖、侵袭、迁移，并促进其凋亡。

Objective Analyze the effect of LncRNA SNHG16 targeted regulation of miR?516a?5p on the proliferation， invasion， and migration ability of colorectal cancer cells. Methods Real time fluorescence RT?PCR was used to detect the expression of lncRNA SNHG16 and miR?516a?5p， and SW480 cells were constructed to inhibit lncRNA SNHG16 expression. SW480 cells were transfected and divided into a NC group， a si?NC group， a si?SNHG16 group， a miR?NC group， a miR?516a?5p group， a si?SNHG16+anti miR?NC group， and a si?SNHG16+anti miR?516a?5p group to detect cell proliferation， apoptosis， invasion， and migration in each group. Results Compared with adjacent tissues， the expression level of lncRNA SNHG16 in colorectal cancer tissue increased， while the expression level of miR?516a?5p decreased （P < 0.05）. Compared with the FHC group， the expression levels of lncRNA SNHG16 and miR?516a?5p were increased in the HCT116， SW620， and SW480 groups， while the expression levels of miR?516a?5p were lower. The SW480 group had the highest lncRNA SNHG16 and the lowest miR?516a?5p levels （P < 0.05）. Compared with the si?NC group， the expression level of lncRNA SNHG16 in the si?SNHG16 group decreased （P < 0.05）， indicating the successful construction of SW480 cell lines that interfered with lncRNA SNHG16 expression. Compared with the si?NC group， the si?SNHG16 group showed a decrease in CyclinD1， MMP?2， MMP?9， OD value， number of migrating and invading cells， and an increase in apoptotic cells （P < 0.05）. Compared with the miR?NC group， the miR?516a?5p group showed an increase in miR?516a?5p expression levels （P < 0.05）， indicating the successful construction of SW480 cell lines with high expression of miR?516a?5p. Compared with the miR?NC group， the miR?516a?5p group showed a decrease in CyclinD1， MMP?2， MMP?9， OD value， number of migrating cells， and number of invasive cells， while an increase in apoptotic cells （P < 0.05）. The dual luciferase report test showed that compared with the miR?NC group， miR?516a?5p could reduce the luciferase activity of SNHG16 （P < 0.05）， and had a small impact on the luciferase activity of MUT?SNHG16 （P > 0.05）. Compared with the si?NC group， inhibiting the expression of lncRNA SNHG16 resulted in an increase in miR?516a?5p expression and apoptotic cells in SW480 cells， as well as a decrease in CyclinD1， MMP?2， MMP?9， OD value， number of migratory cells， and number of invasive cells （P < 0.05）. Compared with the si?SNHG16+anti miR?NC group， the si?SNHG16+anti miR?516a?5p group showed a decrease in miR?516a?5p expression and apoptotic cells， while the cyclinD1， MMP?2， MMP?9， OD value， number of migratory cells， and number of invasive cells increased （P < 0.05）. Conclusion Interfering with lncRNA SNHG16 expression can regulate the expression of miR?516a?5p， inhibit the proliferation， invasion， migration， and promote apoptosis of colorectal cancer cells.