Department of Otolaryngology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Eur Rev Med Pharmacol Sci. 2018 Mar;22(5):1333-1341. doi: 10.26355/eurrev_201803_14475.
To investigate the expression of human long non-coding ribonucleic acid (RNA) small nucleolar RNA host gene 1 (SNHG1) in laryngeal carcinoma tissues, and to study the effect of SNHG1 on biological functions of laryngeal carcinoma HEp-2 cells.
The expression levels of SNHG1 in 20 pairs of laryngeal carcinoma tissues and para-carcinoma tissues were detected via Real-time fluorescence quantitative polymerase chain reaction (PCR). Laryngeal carcinoma cells were transfected with small interfering (si)-SNHG1 transiently using the RNA interference technique. The effects of si-SNHG1 on proliferation, apoptosis, invasion, and migration of laryngeal carcinoma HEp-2 cells were detected via cell counting kit-8 (CCK-8), colony formation assay, flow cytometry, and wound healing and Transwell assay, respectively.
Results of PCR showed that the expression of SNHG1 in carcinoma tissues was increased compared with that in para-carcinoma tissues. Results of CCK-8 and colony formation assay revealed that SNHG1 knockdown could significantly inhibit the proliferation of laryngeal carcinoma HEp-2 cells. Flow cytometry showed that transfection with si-SNHG1 could promote the apoptosis of HEp-2 cells. Moreover, results of wound healing and Transwell assay showed that SNHG1 knockdown could inhibit invasion and migration of HEp-2 cells through inhibiting the epithelial-mesenchymal transition (EMT) process and expressions of matrix metalloproteinase-2 (MMP-2) and MMP-9 in cells.
The expression of SNHG1 in laryngeal carcinoma tissues is significantly higher than that in para-carcinoma tissue. Patients with high expression of SNHG1 have a poor prognosis. SNHG1 knockdown in HEp-2 cells can inhibit cell proliferation, invasion, and metastasis, and can promote apoptosis.
研究人类长非编码 RNA 小核仁 RNA 宿主基因 1（SNHG1）在喉癌组织中的表达，并研究 SNHG1 对喉癌细胞 HEp-2 生物学功能的影响。
采用实时荧光定量聚合酶链反应（PCR）检测 20 对喉癌组织及其癌旁组织中 SNHG1 的表达水平。采用 RNA 干扰技术瞬时转染喉癌细胞 SNHG1 的小干扰（si）-SNHG1。采用细胞计数试剂盒-8（CCK-8）、集落形成实验、流式细胞术以及划痕愈合和 Transwell 实验分别检测 si-SNHG1 对喉癌细胞 HEp-2 增殖、凋亡、侵袭和迁移的影响。
PCR 结果显示，癌组织中 SNHG1 的表达高于癌旁组织。CCK-8 和集落形成实验结果显示，SNHG1 敲低可显著抑制喉癌细胞 HEp-2 的增殖。流式细胞术结果显示，转染 si-SNHG1 可促进 HEp-2 细胞凋亡。此外，划痕愈合和 Transwell 实验结果显示，SNHG1 敲低通过抑制上皮-间质转化（EMT）过程以及细胞中基质金属蛋白酶-2（MMP-2）和 MMP-9 的表达，可抑制 HEp-2 细胞的侵袭和迁移。
喉癌组织中 SNHG1 的表达明显高于癌旁组织。SNHG1 高表达的患者预后不良。HEp-2 细胞中 SNHG1 的敲低可抑制细胞增殖、侵袭和转移，并促进细胞凋亡。
