长链非编码RNA-LncRNA小核仁RNA宿主基因14对乳腺癌细胞增殖和迁移的影响

Effects and mechanisms of Lnc RNA-SNHG14 on proliferation and migration of breast cancer cells

目的探讨长链非编码RNA(long non coding RNAs,LncRNAs) LncRNA小核仁RNA宿主基因14(small nucleolar RNA host gene 14,SNHG14)在乳腺癌组织中的表达水平,及其对乳腺癌细胞增殖和迁移的影响和潜在机制。方法收集于2018年1月至2019年1月于我院行手术治疗的乳腺癌组织和癌旁组织共40例,对比乳腺癌组织和癌旁组织LncRNA SNHG14的表达水平,分析不同乳腺癌细胞系的LncRNA SNHG14表达水平。敲低SNHG14的表达水平后,采用CCK 8检测CAL51细胞的活力,采用Transwell实验检测细胞侵袭和迁移,进一步预测和验证SNHG14的结合miRNA和潜在机制。结果乳腺癌组织和细胞系的SNHG14表达水平显著增高,敲低SNHG14后抑制CAL51细胞的增殖、侵袭和迁移能力,SNHG14潜在与miR 144靶向结合,miR 144低表达与乳腺癌预后不良相关。抑制SNHG14后CAL51细胞的miR 144表达显著下降,而中心体蛋白55(centrosomal protein 55,CEP55)的表达显著升高。结论LncRNA SNHG14在乳腺癌组织和细胞中高表达,LncRNA SNHG14可通过miR 144/CEP55信号轴从而促进乳腺癌细胞的增殖和迁移。

Objective To investigate the expression of LncRNA SNHG14 in breast cancer tissues and its effect on the proliferation and migration of breast cancer cells.Methods A total of 40 breast cancer tissues and paracancerous tissues were collected from our hospital from January 2018 to January 2019.The expression levels of LncRNA SNHG14 in breast cancer tissues and adjacent tissues were compared.The expression level of LncRNA SNHG14 in different breast cancer cell lines were analyzed.After knocking down the expression level of SNHG14,CCK8 was used to detect the viability of CAL51 cells.Transwell assay was used to detect cell invasion and migra tion,further predicting and verifying the binding miRNA and potential mechanism of SNHG14.Results The ex pression level of SNHG14 in breast cancer tissues and cell lines was significantly increased.The knockdown of SN HG14 inhibited the proliferation,invasion and migration of CAL51 cells.SNHG14 potentially binds to miR 144.Low expression of miR 144 related with poor prognosis of breast cancer.The expression of miR 144 in CAL51 cells was significantly decreased after inhibition of SNHG14,while the expression of CEP55 was significantly increased.Conclusion LncRNA SNHG14 is highly expressed in breast cancer tissues and cells,and LncRNA SNHG14 can promote the proliferation and migration of breast cancer cells through the miR 144/CEP55 signal axis.