长链非编码RNA SLC25A25-AS1对喉癌细胞侵袭和迁移的影响及其机制
孙倩, 刘盛力, 马钰, 杜莉中国医科大学附属第四医院耳鼻咽喉科, 沈阳 110032
收稿日期:
2021-12-06出版日期:
2022-04-20发布日期:
2022-05-05通讯作者:
杜莉E-mail:duli_ent@163.com作者简介:
孙倩(1989-),女,医师,硕士研究生.基金资助:
辽宁省自然科学基金 (20170541000)关键词: 喉癌, 长链非编码RNA, SLC25A25-AS1, 信号转导及转录激活因子3, 血管内皮生长因子
Abstract: Objective To investigate the effect of antisense RNA1 of long noncoding RNA (lncRNA) SLC25A25 (SLC25A25-AS1) on the invasion and migration of laryngeal carcinoma cells and its mechanism. Methods The levels of SLC25A25-AS1 in human nasopharyngeal epithelial cells NP69 and laryngeal carcinoma cells TU-212,TU-177,and Hep-2 were detected by real-time fluorescent quantitative polymerase chain reaction. The proliferation activity,scratch healing rate,and number of membrane-penetrating cells were measured by MTT,scratch-wound,and Transwell assays,respectively. The expressions of signal transduction and activator of transcription 3 (STAT3),p-STAT3,and vascular endothelial growth factor (VEGF) proteins were detected by Western blotting. Results The level of SLC25A25-AS1 in laryngeal cancer cells was significantly lower than that in NP69 cells (P < 0.05). Overexpression of SLC25A25-AS1 significantly reduced the proliferation,migration,and invasion activity of HEP-2 cells (P < 0.05). The levels of p-STAT3 and VEGF proteins in HEP-2 cells after SLC25A25-AS1 overexpression significantly decreased (P < 0.05). Conclusion SLC25A25-AS1 overexpression can inhibit the proliferation,migration,and invasion of laryngeal cancer Hep-2 cells,and this tumor suppressive effect may be through the STAT3/VEGF pathway.
Key words: laryngeal carcinoma, long noncoding RNA, SLC25A25-AS1, signal transduction and activator of transcription 3, vascular endothelial growth factor
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