| 张金娜.LncRNA SNHG16调节miR-20a-5p/LIMK1轴对子宫内膜癌细胞增殖、侵袭和迁移的影响[J].安徽医药,待发表. |
| LncRNA SNHG16调节miR-20a-5p/LIMK1轴对子宫内膜癌细胞增殖、侵袭和迁移的影响 |
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| 投稿时间：2026-06-09 录用日期：2026-08-10 |
| DOI： |
| 中文关键词: 长链非编码小核仁RNA宿主基因16 微小RNA-20a-5p LIM域激酶1 子宫内膜癌 增殖 迁移 侵袭 |
| 英文关键词: |
| 基金项目:河北省卫生健康委项目(编号:20241000) |
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| 摘要点击次数: 30 |
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| 中文摘要: |
| 目的 探索长链非编码小核仁RNA宿主基因16（LncRNA SNHG16）能否通过调控微小RNA-20a-5p（miR-20a-5p）/LIM域激酶1（LIMK1）轴抑制子宫内膜癌细胞恶性生物学行为。方法 取子宫内膜癌患者癌组织、癌旁组织及人子宫内膜上皮细胞、人子宫内膜癌细胞HEC-1A，qRT-PCR检测组织及细胞中SNHG16、miR-20a-5p和LIMK1 mRNA水平；免疫组化实验检测子宫内膜癌组织及癌旁组织LIMK1蛋白表达；并将HEC-1A细胞分别转染不同质粒，命名为Control组、si-NC组、si-SNHG16组、si-SNHG16+anti-miR-NC组和si-SNHG16+anti-miR-20a-5p组；分别采用平板克隆、MTT、划痕实验、Transwell、流式细胞仪、Western blot检测细胞恶性生物行为、细胞凋亡及LIMK1、p-Cofilin蛋白表达水平，并采用双荧光素酶、RNA pull-down和RIP实验验证SNHG16与miR-20a-5p、miR-20a-5p与LIMK1靶向关系。结果 相较于癌旁组织，子宫内膜癌组织中SNHG16、LIMK1 mRNA表达水平均升高，miR-20a-5p表达水平降低（P＜0.05）；与子宫内膜上皮细胞进行比较，HEC-1A细胞SNHG16和LIMK1 mRNA表达水平均升高，而miR-20a-5p表达水平降低（P＜0.05）；相较于si-NC组，si-SNHG16组细胞中SNHG16、LIMK1 mRNA、LIMK1及p-Cofilin蛋白表达量均呈现下降趋势，且细胞存活率、细胞相对集落数、侵袭细胞数和迁移距离均显著减少，miR-20a-5p表达量及细胞凋亡率均增加（P＜0.05）；相较于si-SNHG16+anti-miR-NC组，si-SNHG16+anti-miR-20a-5p组细胞中miR-20a-5p表达量下降，细胞凋亡率减少，而LIMK1 mRNA、LIMK1及p-Cofilin蛋白表达量增加，细胞存活率、细胞相对集落数、侵袭细胞数和细胞迁移距离均显著增加（P＜0.05）。结论 下调LncRNA SNHG16通过调控miR-20a-5p/LIMK1轴抑制子宫内膜癌细胞增殖、侵袭和迁移。 |
| 英文摘要: |
| Objective To investigate whether long non-coding small nucleolar RNA host gene 16 (LncRNA SNHG16) can inhibit the malignant biological behaviors of endometrial cancer cells by regulating the microRNA-20a-5p (miR-20a-5p)/LIM domain kinase 1 (LIMK1) axis. Methods Cancer tissues and paracancerous tissues from patients with endometrial cancer, as well as human normal endometrial epithelial cells and human endometrial cancer HEC-1A cells, were collected. The mRNA expression levels of SNHG16, miR-20a-5p and LIMK1 in tissues and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemistry was used to detect LIMK1 protein expression in endometrial cancer tissues and adjacent non-cancerous tissues. HEC-1A cells were transfected with different plasmids and divided into five groups: Control group, si-NC group, si-SNHG16 group, si-SNHG16+anti-miR-NC group and si-SNHG16+anti-miR-20a-5p group. The malignant biological behaviors, apoptosis, and protein expression levels of LIMK1 and p-Cofilin were detected by colony formation assay, MTT assay, scratch wound healing assay, Transwell assay, flow cytometry, and Western blot, respectively. The dual-luciferase reporter assay, RNA pull-down assay, and RIP assay were performed to verify the targeted relationships between SNHG16 and miR-20a-5p, as well as between miR-20a-5p and LIMK1. Results Compared with paracancerous tissues, the mRNA expression levels of SNHG16 and LIMK1 were significantly increased, while the expression level of miR-20a-5p was significantly decreased in endometrial cancer tissues (P＜0.05). In comparison with normal endometrial epithelial cells, HEC-1A cells showed significantly higher mRNA expression levels of SNHG16 and LIMK1 and a markedly lower expression level of miR-20a-5p (P＜0.05). Compared with the si-NC group, the si-SNHG16 group exhibited significant reductions in the mRNA expression levels of SNHG16 and LIMK1, the protein expression levels of LIMK1 and p-Cofilin, cell viability, relative colony formation number, invasive cell number and migration distance, along with significant elevations in miR-20a-5p expression level and cell apoptosis rate (P＜0.05). In contrast to the si-SNHG16+anti-miR-NC group, the si-SNHG16+anti-miR-20a-5p group had a significantly decreased miR-20a-5p expression level and cell apoptosis rate, whereas the mRNA expression level of LIMK1, the protein expression levels of LIMK1 and p-Cofilin, cell viability, relative colony formation number, invasive cell number and cell migration distance were significantly increased (P＜0.05). Conclusion Down-regulation of LncRNA SNHG16 inhibits the proliferation, invasion and migration of endometrial cancer cells by regulating the miR-20a-5p/LIMK1 axis. |
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