Hsa_circ_0057104, by competitive adsorption of miR-627-5p, mediates CCND2 expression to promote malignant proliferation and Warburg effect of colorectal cancer.

IF 6.5 3区工程技术 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Biotechnology & Genetic Engineering Reviews Pub Date : 2024-12-01 Epub Date: 2023-05-02 DOI:10.1080/02648725.2023.2199243

Lin Zhang, Jian Xu, Dequan Jiang, Jing Zhang, Hongyuan Li, Zhengzhong Zhao, Zhechuan Mei

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引用次数: 0

Abstract

Objective: hsa_circ_0057104 (circPDK1) has been elucidated to regulate malignant behavior in pancreatic and renal cell carcinoma. The study functionally aimed at how circPDK1 modifies colorectal cancer (CRC) progression, along with its potential molecular mechanism.

Methods: circPDK1 expression patterns in CRC tissues and cell lines were analyzed by RT-qPCR. circPDK1/miR-627-5p/CCND2 expression levels were changed by transient transfection. CCK-8 assay, flow cytometry, Transwell, immunoblotting, and commercial kits were utilized to measure CRC cell proliferation, apoptosis, invasion/migration, and glycolysis processes. Dual luciferase reporting assay and RIP assay were employed to evaluate the targeting relationship between circPDK1/miR-627-5p/CCND2.

Results: circPDK1 was highly expressed in CRC. circPDK1 knockdown inhibited CRC cell proliferation, invasion/migration, and warburg effect and forced apoptosis. Overexpressing circPDK1 had the opposite effect. The effects of circPDK1 knockdown or circPDK1 overexpression on CRC cells were mitigated by downregulating miR-627-5p or CCND2, respectively. CircPDK1, by competitive adsorption of miR-627-5p, mediated CCND2 expression.

Conclusion: CircPDK1 induces the malignant behavior of CRC by competitive adsorption of miR-627-5p mediating CCND2 expression, offering new insights into the future development of CRC-targeted drugs.

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Hsa_circ_0057104 通过竞争性吸附 miR-627-5p，介导 CCND2 的表达，促进结直肠癌的恶性增殖和沃伯格效应。

目的：已阐明hsa_circ_0057104（circPDK1）可调控胰腺癌和肾细胞癌的恶性行为。本研究旨在从功能上探讨 circPDK1 如何改变结直肠癌（CRC）的进展及其潜在的分子机制。方法：通过 RT-qPCR 分析 circPDK1 在 CRC 组织和细胞系中的表达模式；通过瞬时转染改变 circPDK1/miR-627-5p/CCND2 的表达水平。利用 CCK-8 检测法、流式细胞术、Transwell、免疫印迹法和商业试剂盒检测 CRC 细胞的增殖、凋亡、侵袭/迁移和糖酵解过程。结果显示：circPDK1在CRC中高表达，敲除circPDK1可抑制CRC细胞增殖、侵袭/迁移、沃伯格效应和强迫凋亡。而过表达circPDK1则会产生相反的效果。分别通过下调miR-627-5p或CCND2可减轻circPDK1敲除或circPDK1过表达对CRC细胞的影响。CircPDK1通过竞争性吸附miR-627-5p，介导了CCND2的表达：结论：CircPDK1通过竞争性吸附miR-627-5p介导CCND2的表达，诱导了CRC的恶性行为，为今后开发CRC靶向药物提供了新的思路。

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

Biotechnology & Genetic Engineering Reviews BIOTECHNOLOGY & APPLIED MICROBIOLOGY-GENETICS & HEREDITY

CiteScore

6.50

自引率

3.10%

发文量

期刊介绍： Biotechnology & Genetic Engineering Reviews publishes major invited review articles covering important developments in industrial, agricultural and medical applications of biotechnology.