CircKRT14 upregulates E2F3 by interacting with miR-1256 to act as an oncogenic factor in esophageal cancer.

IF 2.7 4区医学 Q3 TOXICOLOGY

Human & Experimental Toxicology Pub Date : 2023-01-01 DOI:10.1177/09603271231155093

Xingzhuo Guan, Tingzhu Lan, Yuanshi Wang, Yan Cui, Jinyu Duan, Hongjun Xu

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Abstract

Background: A growing number of studies have focused on the regulatory role of circular RNAs (circRNAs) in a variety of cancers. The purpose of this study was to investigate the effect of circRNA Keratin 14 (circKRT14) on the progression of esophageal cancer (EC).

Methods: The levels of circKRT14, miR-1256 and E2F transcription factor 3 (E2F3) were analyzed by real-time quantitative polymerase chain reaction (qRT-PCR) and western blot. The circular structure of circKRT14 was confirmed by RNase R digestion assay. Cell apoptosis, migration and invasion were detected by flow cytometry and transwell assay. The protein levels of related factors were determined by western blot. The relationship between miR-1256 and circKRT14 or E2F3 was verified by dual-luciferase reporter assay. The in vivo function of circKRT14 was studied by xenograft tumor assay.

Results: CircKRT14 was significantly increased in EC tissues and cells. CircKRT14 silencing inhibited EC cell proliferation, migration, and invasion, but promoted EC cell apoptosis in vitro. CircKRT1 acted as a sponge for miR-1256 in EC, and in-miR-1256 abolished the inhibitory effect of circKRT14 suppression on EC cell progression. E2F3 was a target of miR-1256 and functioned as an oncogene in EC cells. MiR-1256 curbed EC progression by downregulating E2F3. CircKRT14 could affect E2F3 expression by targeting miR-1256. CircKRT14 regulated EC progression in vivo through miR-1256/E2F3 axis.

Conclusions: These results uncovered that circKRT14 up-regulated the expression of E2F3 and promoted the malignant development of EC through sponging miR-1256.

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CircKRT14通过与miR-1256相互作用上调E2F3，作为食管癌的致癌因子。

背景:越来越多的研究关注环状rna (circRNAs)在多种癌症中的调节作用。本研究的目的是探讨circRNA角蛋白14 (circKRT14)在食管癌(EC)进展中的作用。方法:采用实时定量聚合酶链式反应(qRT-PCR)和western blot分析circKRT14、miR-1256和E2F转录因子3 (E2F3)水平。RNase R酶切实验证实了circKRT14的环状结构。流式细胞术和transwell法检测细胞凋亡、迁移和侵袭。western blot检测相关因子蛋白水平。通过双荧光素酶报告基因检测验证miR-1256与circKRT14或E2F3之间的关系。通过异种移植肿瘤实验研究circKRT14的体内功能。结果:CircKRT14在EC组织和细胞中显著升高。CircKRT14沉默抑制EC细胞增殖、迁移和侵袭，但促进EC细胞体外凋亡。CircKRT1在EC中充当miR-1256的海绵，in-miR-1256消除了circKRT14抑制EC细胞进展的抑制作用。E2F3是miR-1256的靶点，在EC细胞中作为癌基因发挥作用。MiR-1256通过下调E2F3抑制EC进展。CircKRT14可以通过靶向miR-1256影响E2F3的表达。CircKRT14通过miR-1256/E2F3轴调控EC在体内的进展。结论:这些结果揭示circKRT14通过海绵化miR-1256上调E2F3的表达，促进EC的恶性发展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Human & Experimental Toxicology 医学-毒理学

CiteScore

5.70

自引率

3.60%

发文量

128

审稿时长

2.3 months

期刊介绍： Human and Experimental Toxicology (HET), an international peer reviewed journal, is dedicated to publishing preclinical and clinical original research papers and in-depth reviews that comprehensively cover studies of functional, biochemical and structural disorders in toxicology. The principal aim of the HET is to publish timely high impact hypothesis driven scholarly work with an international scope. The journal publishes on: Structural, functional, biochemical, and molecular effects of toxic agents; Studies that address mechanisms/modes of toxicity; Safety evaluation of novel chemical, biotechnologically-derived products, and nanomaterials for human health assessment including statistical and mechanism-based approaches; Novel methods or approaches to research on animal and human tissues (medical and veterinary patients) investigating functional, biochemical and structural disorder; in vitro techniques, particularly those supporting alternative methods