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长链非编码 RNA VPS9D1-AS1 通过海绵吸附 miR-1301-3p 和 CLDN1 促进结肠腺癌的生长。

Long non-coding RNA VPS9D1-AS1 promotes growth of colon adenocarcinoma by sponging miR-1301-3p and CLDN1.

机构信息

Department of Gastroenterology, The First Affiliated Hospital, Zhengzhou University, No.1, Jianshe East Road, Erqi District, Zhengzhou, 450052, Henan, China.

出版信息

Hum Cell. 2021 Nov;34(6):1775-1787. doi: 10.1007/s13577-021-00604-1. Epub 2021 Sep 14.

Abstract

Colon adenocarcinoma is a frequent malignancy among all colon cancer types. Long non-coding RNAs (lncRNAs) are involved in the progression of colon adenocarcinoma. This study aimed to uncover the molecular mechanism of VPS9D1-AS1 in regulating colon adenocarcinoma development. Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) revealed that VPS9D1-AS1 expression was markedly upregulated in colon adenocarcinoma tissues and cell lines. Cell functional experiments showed that knockdown of VPS9D1-AS1 repressed the growth and invasion of colon adenocarcinoma cells but upregulated cell apoptosis. In addition, we confirmed the interaction of VPS9D1-AS1-miR-1301-3p-CLDN1 using a luciferase assay. Downregulation of miR-1301-3p promoted the progression of colon adenocarcinoma cells. In conclusion, VPS9D1-AS1 facilitated cell growth and suppressed apoptosis of colon adenocarcinoma cells by sponging miR-1301-3p and upregulating CLDN1, which may be effective therapeutic strategies for patients with colon adenocarcinoma.

摘要

结肠腺癌是所有结肠癌类型中常见的恶性肿瘤。长链非编码 RNA(lncRNA)参与了结肠腺癌的进展。本研究旨在揭示 VPS9D1-AS1 在调节结肠腺癌发展中的分子机制。定量逆转录聚合酶链反应(RT-qPCR)显示 VPS9D1-AS1 在结肠腺癌组织和细胞系中表达明显上调。细胞功能实验表明,VPS9D1-AS1 的敲低抑制了结肠腺癌细胞的生长和侵袭,但上调了细胞凋亡。此外,我们使用荧光素酶测定证实了 VPS9D1-AS1-miR-1301-3p-CLDN1 的相互作用。miR-1301-3p 的下调促进了结肠腺癌细胞的进展。总之,VPS9D1-AS1 通过海绵 miR-1301-3p 和上调 CLDN1 促进结肠腺癌细胞的生长并抑制细胞凋亡,这可能是结肠腺癌患者的有效治疗策略。

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