SP1 诱导的 circ_0017552 通过上调 NET1 调节结肠癌细胞的增殖和凋亡

IF 1.4 4区 医学 Q4 GENETICS & HEREDITY
Daocheng Liu, Minmin Shen, Zhaohui Liu, Dong Chen, Yuan Pan, Lei Zhang, Xiaoping Xu
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引用次数: 0

摘要

结肠癌(CC)是全球常见的恶性肿瘤,近年来在中国的发病率和死亡率明显上升。癌症的分子功能逐渐成为癌症研究的热点。据报道,神经上皮细胞转化1(NET1)是前列腺癌和胃癌的诱因之一。我们的研究发现,NET1在CC细胞中过表达。然后,功能缺失试验发现,NET1 能促进 CC 细胞增殖,抑制 CC 细胞凋亡。接着,miR-338-3p 被证实靶向 NET1。之后,我们又验证了源自 NET1 的 circ_0017552 可以正向调节 NET1 的表达。此外,circ_0017552还是 miR-338-3p 的海绵。拯救实验结果表明,circ_0017552能通过上调NET1来调控CC细胞的增殖和凋亡。研究发现,circ_0017552中存在一种名为Sp1(SP1)的转录因子。SP1诱导circ_0017552的转录,从而促进CC细胞增殖并抑制CC细胞凋亡。总之,SP1诱导的circ_0017552通过miR-338-3p/NET1轴调控CC细胞的增殖和凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
SP1-induced circ_0017552 modulates colon cancer cell proliferation and apoptosis via up-regulation of NET1

Colon cancer (CC) is a common malignancy over the world and its morbidity and mortality significantly went up in China in recent years. Molecular functions in cancers have gradually been the pivot subject in cancer research. Neuroepithelial cell transforming 1 (NET1) was reported to contribute to prostate cancer and gastric cancer. Our study figured out that NET1 was overexpressed in CC cells. Then, loss-of-function assays revealed that NET1 facilitated CC cell proliferation and repressed CC cell apoptosis. Next, miR-338–3p was confirmed to target NET1. After that, we verified that circ_0017552 which originates from NET1 could positively modulate NET1 expression. Besides, circ_0017552 was a sponge of miR-338–3p. Rescue assays’ results demonstrated that circ_0017552 could regulate CC cell proliferation and apoptosis through up-regulation of NET1. A transcription factor named Sp1 (SP1) was found to be present in circ_0017552. SP1 induced transcription of circ_0017552 to facilitate CC cell proliferation and inhibit CC cell apoptosis. In a word, SP1-induced circ_0017552 regulated CC cell proliferation and apoptosis through miR-338–3p/NET1 axis.

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来源期刊
Cancer Genetics
Cancer Genetics ONCOLOGY-GENETICS & HEREDITY
CiteScore
3.20
自引率
5.30%
发文量
167
审稿时长
27 days
期刊介绍: The aim of Cancer Genetics is to publish high quality scientific papers on the cellular, genetic and molecular aspects of cancer, including cancer predisposition and clinical diagnostic applications. Specific areas of interest include descriptions of new chromosomal, molecular or epigenetic alterations in benign and malignant diseases; novel laboratory approaches for identification and characterization of chromosomal rearrangements or genomic alterations in cancer cells; correlation of genetic changes with pathology and clinical presentation; and the molecular genetics of cancer predisposition. To reach a basic science and clinical multidisciplinary audience, we welcome original full-length articles, reviews, meeting summaries, brief reports, and letters to the editor.
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