[LncRNA SNHG15通过海绵吸附miR-30b-3p调控COX6B1促进肺腺癌细胞的增殖、迁移和侵袭]。

Q3 Medicine
Xiuying Gong, Shunfu Hou, Miaomiao Zhao, Xiaona Wang, Zhihan Zhang, Qinghua Liu, Chonggao Yin, Hongli Li
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引用次数: 0

摘要

目的:探讨lncRNA SNHG15调控肺腺癌细胞增殖、侵袭和迁移的分子机制。方法:利用lncRNA微阵列芯片数据集GSE196584和lncrbase预测与miR-30b-3p相互作用的lncRNA,并利用在线数据库研究其与患者预后的相关性,选择lncRNA核仁RNA宿主基因15 (SNHG15)进行进一步分析。采用荧光原位杂交和qRT-PCR检测lncRNA SNHG15的亚细胞定位及其在正常人肺上皮细胞和肺腺癌细胞系中的表达水平。在培养的A549细胞中,转染SNHG15敲低质粒(sh-SNHG15)、miR-30b-3p抑制剂或它们共同转染后,用EdU、伤口愈合和Transwell试验评估细胞增殖、迁移和侵袭的变化。利用生物信息学分析预测lncRNA SNHG15与COX6B1之间的调控关系,并在转染sh-SNHG15、COX6B1过表达质粒或两者同时转染的A549细胞中,通过Western blotting和拯救实验对结果进行验证。结果:LncRNA SNHG15可靶向miR-30b-3p,前者在肺腺癌中高表达,且与患者预后差相关。LncRNA SNHG15定位于细胞质中,在A549和NCI-H1299细胞中的表达水平高于BEAS-2B细胞。在A549细胞中,lncRNA SNHG15敲低可显著抑制细胞迁移、侵袭和增殖,miR-30b-3p抑制剂可逆转这些变化。lncRNA SNHG15与COX6B1之间存在调控关系,且两者表达水平呈正相关(r=0.128, P=0.003)。MiR-30b-3p敲低明显降低A549细胞中COX6B1的表达,过表达COX6B1使细胞摆脱lncRNA-SNHG15敲低的抑制作用。结论:LncRNA SNHG15可能通过ceRNA机制与COX6B1竞争结合miR-30b-3p,影响肺腺癌细胞的增殖、迁移和侵袭。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[LncRNA SNHG15 promotes proliferation, migration and invasion of lung adenocarcinoma cells by regulating COX6B1 through sponge adsorption of miR-30b-3p].

Objectives: To explore the molecular mechanism by which lncRNA SNHG15 regulates proliferation, invasion and migration of lung adenocarcinoma cells.

Methods: The lncRNA microarray chip dataset GSE196584 and LncBase were used to predict the lncRNAs that interact with miR-30b-3p, and their association with patient prognosis were investigated using online databases, after which lncRNA nucleolar RNA host gene 15 (SNHG15) was selected for further analysis. The subcellular localization of lncRNA SNHG15 and its expression levels in normal human lung epithelial cells and lung adenocarcinoma cell lines were detected using fluorescence in situ hybridization and qRT-PCR. In cultured A549 cells, the changes in cell proliferation, migration, and invasion following transfection with a SNHG15 knockdown plasmid (sh-SNHG15), a miR-30b-3p inhibitor, or their co-transfection were assessed with EdU, wound healing, and Transwell assays. Bioinformatics analyses were used to predict the regulatory relationship between lncRNA SNHG15 and COX6B1, and the results were verified using Western blotting and rescue experiments in A549 cells transfected with sh-SNHG15, a COX6B1-overexpressing plasmid, or both.

Results: LncRNA SNHG15 was shown to target miR-30b-3p, and the former was highly expressed in lung adenocarcinoma, and associated with a poor patient prognosis. LncRNA SNHG15 was localized in the cytoplasm and expressed at higher levels in A549 and NCI-H1299 cells than in BEAS-2B cells. In A549 cells, lncRNA SNHG15 knockdown significantly inhibited cell migration, invasion and proliferation, and these changes were reversed by miR-30b-3p inhibitor. A regulatory relationship was found between lncRNA SNHG15 and COX6B1, and their expression levels were positively correlated (r=0.128, P=0.003). MiR-30b-3p knockdown obviously decreased COX6B1 expression in A549 cells, and COX6B1 overexpression rescued the cells from the inhibitory effects of lncRNA-SNHG15 knockdown.

Conclusions: LncRNA SNHG15 may compete with COX6B1 to bind miR-30b-3p through a ceRNA mechanism to affect proliferation, migration, and invasion of lung adenocarcinoma cells.

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南方医科大学学报杂志
南方医科大学学报杂志 Medicine-Medicine (all)
CiteScore
1.50
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0.00%
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208
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