SNHG17通过调节CXCL12介导的血管生成促进结肠直肠腺癌细胞的增殖和迁移。
SNHG17 promotes the proliferation and migration of colorectal adenocarcinoma cells by modulating CXCL12-mediated angiogenesis.
作者信息
Liu Yang, Li Qinshan, Tang Dongxin, Li Mengxing, Zhao Peng, Yang Wenxiu, Shu Liping, Wang Jishi, He Zhixu, Li Yanju, Wang Feiqing
机构信息
Department of Science and Education, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, No. 71 Bao Shan North Road, Yunyan District, Guiyang, 550001, Guizhou, China.
National & Guizhou Joint Engineering Laboratory for Cell Engineering and Biomedicine Technique, Guizhou Medical University, Guiyang, 550004, Guizhou, China.
出版信息
Cancer Cell Int. 2020 Nov 26;20(1):566. doi: 10.1186/s12935-020-01621-0.
BACKGROUND
Colorectal adenocarcinoma (CRA) is one of the leading causes of cancer-related deaths in the world. Long non-coding RNAs (lncRNAs) have been implicated to be effective regulators in the disease course of human cancers, including CRA. Small nucleolar RNA host gene 17 (SNHG17) belongs to lncRNAs, and it has been reported in breast cancer and gastric cancer. However, the function of SNHG17 and its mechanism in CRA progression remain largely unknown. In this study, we attended to shedding some light on the role of SNHG17 in CRA.
METHODS
RT-qPCR was used to assess SNHG17 expression in CRA cells. CCK-8 assay, colony formation and transwell assay were carried out to detect the regulatory effect of SNHG17 silencing on CRA cell proliferation and migration. The angiogenesis of SNHG7-downregulated CRA cells was analyzed by tube formation assay. Mechanism experiments were conducted to identify the interaction between miR-23a-3p and SNHG17 or C-X-C motif chemokine ligand 12 (CXCL12).
RESULTS
SNHG17 possessed with high expression in CRA cells. Knockdown of SNHG17 caused the inhibition on CRA cell proliferation and migration. SNHG17 promoted CRA cell proliferation and migration by sponging miR-23a-3p to upregulate CXCL12.
CONCLUSION
SNHG17 promotes the proliferation and migration of CRA cells by inhibiting miR-23a-3p to modulate CXCL12-mediated angiogenesis.
背景
结直肠癌（CRA）是全球癌症相关死亡的主要原因之一。长链非编码RNA（lncRNA）被认为是人类癌症（包括CRA）病程中的有效调节因子。小核仁RNA宿主基因17（SNHG17）属于lncRNA，在乳腺癌和胃癌中已有报道。然而，SNHG17在CRA进展中的功能及其机制仍 largely unknown。在本研究中，我们试图阐明SNHG17在CRA中的作用。
方法
采用RT-qPCR评估CRA细胞中SNHG17的表达。进行CCK-8检测、集落形成和Transwell检测，以检测SNHG17沉默对CRA细胞增殖和迁移的调节作用。通过管腔形成试验分析SNHG7下调的CRA细胞的血管生成。进行机制实验以确定miR-23a-3p与SNHG17或C-X-C基序趋化因子配体12（CXCL12）之间的相互作用。
结果
SNHG17在CRA细胞中高表达。敲低SNHG17导致对CRA细胞增殖和迁移的抑制。SNHG17通过海绵吸附miR-23a-3p上调CXCL12来促进CRA细胞增殖和迁移。
结论
SNHG17通过抑制miR-23a-3p调节CXCL12介导的血管生成来促进CRA细胞的增殖和迁移。
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