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Circ_0084615促进肝细胞癌中上皮-间质转化介导的肿瘤进展。

Circ_0084615 promotes epithelial-mesenchymal transition-mediated tumor progression in hepatocellular carcinoma.

作者信息

Wu Yu, Peng Li

机构信息

Department of Surgical Teaching and Research Hebei Medical University Shi Jiazhuang Hebei China.

Department of Hepatobiliary Surgery The Fourth Hospital of Hebei Medical University Shi Jiazhuang Hebei China.

出版信息

Ann Gastroenterol Surg. 2024 Jun 3;8(6):1107-1117. doi: 10.1002/ags3.12828. eCollection 2024 Nov.

DOI:10.1002/ags3.12828
PMID:39502735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11533029/
Abstract

AIM

CircRNAs have been identified as crucial regulators in tumorigenesis and progression. This study aimed to explore the biological role and underlying mechanism of circ_0084615 in hepatocellular carcinoma (HCC).

METHODS

The expression of RNAs was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The effects of circ_0084615 silencing on malignant behaviors of HCC cells were assessed by CCK-8, colony formation, wound healing, and Transwell assays in vitro and tumor transplantation experiment in vivo. The expression of proteins was detected by Western blotting. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation were performed to explore the mechanism of circ_0084615.

RESULTS

A significant upregulation of circ_0084615 was observed in HCC tissues, and positively correlated with the TNM staging. Silencing of circ_0084615 impeded HCC cell viability, colony formation, migration, invasion, epithelial-mesenchymal transition, and xenograft tumor growth. Mechanistically, circ_0084615 could bind to miR-1200 and eliminate its ability to destroy actin-like 6A (ACTL6A) mRNA, thereby increasing ACTL6A expression and facilitating the malignant behaviors of HCC cells.

CONCLUSIONS

This study clarified the oncogenic activity and mechanism of circ_0084615, thereby providing potential diagnostic biomarker and therapeutic target for inhibiting HCC progression.

摘要

目的

环状RNA（circRNAs）已被确定为肿瘤发生和进展的关键调节因子。本研究旨在探讨circ_0084615在肝细胞癌（HCC）中的生物学作用及潜在机制。

方法

采用定量逆转录-聚合酶链反应（qRT-PCR）检测RNA表达。通过CCK-8、集落形成、伤口愈合和Transwell实验体外评估circ_0084615沉默对HCC细胞恶性行为的影响，并通过体内肿瘤移植实验进行评估。采用蛋白质印迹法检测蛋白质表达。进行双荧光素酶报告基因检测和RNA结合蛋白免疫沉淀以探讨circ_0084615的机制。

结果

在HCC组织中观察到circ_0084615显著上调，且与TNM分期呈正相关。circ_0084615沉默可抑制HCC细胞活力、集落形成、迁移、侵袭、上皮-间质转化及异种移植肿瘤生长。机制上，circ_0084615可与miR-1200结合并消除其破坏肌动蛋白样6A（ACTL6A）mRNA的能力，从而增加ACTL6A表达并促进HCC细胞的恶性行为。

结论

本研究阐明了circ_0084615的致癌活性和机制，从而为抑制HCC进展提供了潜在的诊断生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/462ab89a09bb/AGS3-8-1107-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/8f8952c808ea/AGS3-8-1107-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/f4ebe7f53edc/AGS3-8-1107-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/edd426b61bb7/AGS3-8-1107-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/b4437d77921a/AGS3-8-1107-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/2627770d5ef4/AGS3-8-1107-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/462ab89a09bb/AGS3-8-1107-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/8f8952c808ea/AGS3-8-1107-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/f4ebe7f53edc/AGS3-8-1107-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/edd426b61bb7/AGS3-8-1107-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/b4437d77921a/AGS3-8-1107-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/2627770d5ef4/AGS3-8-1107-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2610/11533029/462ab89a09bb/AGS3-8-1107-g007.jpg

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