LncRNA CCAT2 promotes the proliferation and metastasis of colorectal cancer through activation of the ERK and Wnt signaling pathways by regulating GNB2 expression

IF 2.9 2区医学 Q2 ONCOLOGY

Cancer Medicine Pub Date : 2024-09-03 DOI:10.1002/cam4.70169

Jinhai Tian, Xu Cao, Zongying Jiang, Jia Wang, Wan Fan, Shaoting Zhang, Sien Zhao, Jianmin Sun

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Abstract

Background

Colorectal cancer (CRC) is a prevalent and lethal tumor, with metastasis being the leading cause of mortality. Previous research has indicated that the long non-coding RNA (lncRNA) CCAT2 is involved in the regulation of various tumor progression mechanisms. However, the precise role of CCAT2 in CRC proliferation and metastasis remains ambiguous. This study seeks to elucidate the mechanisms through which CCAT2 influences CRC.

Methods

High-throughput sequencing and RT-qPCR were used to detect CCAT2 expression in CRC. Functional analyses including CCK8, colony formation, wound healing migration, transwell chamber, and Muse® Cell Analyzer assays were performed to study the effects of CCAT2 gene deletion on CRC cells. RNA-pulldown and protein mass spectrometry were employed to identify the interaction between CCAT2 and GNB2 protein.

Results

Increased CCAT2 expression was found in CRC, especially in metastatic CRC. Deletion of CCAT2 gene inhibited CRC cell proliferation, migration, and invasion while promoting apoptosis. The interaction between CCAT2 and GNB2 protein was shown to modulate GNB2 protein alterations and affect the ERK and Wnt signaling pathways, thereby promoting CRC proliferation and metastasis.

Conclusion

CCAT2 plays a crucial role in CRC progression by modulating the ERK and Wnt signaling pathways through its interaction with GNB2. These findings highlight the importance of CCAT2 as a key regulatory element in the mechanisms underlying CRC proliferation and metastasis.

Abstract Image

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LncRNA CCAT2通过调控GNB2的表达，激活ERK和Wnt信号通路，从而促进结直肠癌的增殖和转移。

背景：结直肠癌（CRC）是一种常见的致死性肿瘤，转移是导致死亡的主要原因。以往的研究表明，长非编码 RNA（lncRNA）CCAT2 参与调控各种肿瘤进展机制。然而，CCAT2 在 CRC 增殖和转移中的确切作用仍不明确。本研究试图阐明CCAT2影响CRC的机制。方法：采用高通量测序和RT-qPCR检测CCAT2在CRC中的表达。为研究CCAT2基因缺失对CRC细胞的影响，进行了功能分析，包括CCK8、集落形成、伤口愈合迁移、跨孔室和Muse®细胞分析仪检测。采用RNA-pulldown和蛋白质质谱鉴定CCAT2和GNB2蛋白之间的相互作用：结果：CCAT2在CRC中表达增加，尤其是在转移性CRC中。CCAT2基因缺失可抑制CRC细胞的增殖、迁移和侵袭，同时促进细胞凋亡。研究表明，CCAT2与GNB2蛋白之间的相互作用可调节GNB2蛋白的改变，影响ERK和Wnt信号通路，从而促进CRC的增殖和转移：结论：CCAT2通过与GNB2的相互作用调节ERK和Wnt信号通路，在CRC进展过程中发挥着至关重要的作用。这些发现凸显了CCAT2作为CRC增殖和转移机制中的关键调控因子的重要性。

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

Cancer Medicine ONCOLOGY-

CiteScore

5.50

自引率

2.50%

发文量

907

审稿时长

19 weeks

期刊介绍： Cancer Medicine is a peer-reviewed, open access, interdisciplinary journal providing rapid publication of research from global biomedical researchers across the cancer sciences. The journal will consider submissions from all oncologic specialties, including, but not limited to, the following areas: Clinical Cancer Research Translational research ∙ clinical trials ∙ chemotherapy ∙ radiation therapy ∙ surgical therapy ∙ clinical observations ∙ clinical guidelines ∙ genetic consultation ∙ ethical considerations Cancer Biology: Molecular biology ∙ cellular biology ∙ molecular genetics ∙ genomics ∙ immunology ∙ epigenetics ∙ metabolic studies ∙ proteomics ∙ cytopathology ∙ carcinogenesis ∙ drug discovery and delivery. Cancer Prevention: Behavioral science ∙ psychosocial studies ∙ screening ∙ nutrition ∙ epidemiology and prevention ∙ community outreach. Bioinformatics: Gene expressions profiles ∙ gene regulation networks ∙ genome bioinformatics ∙ pathwayanalysis ∙ prognostic biomarkers. Cancer Medicine publishes original research articles, systematic reviews, meta-analyses, and research methods papers, along with invited editorials and commentaries. Original research papers must report well-conducted research with conclusions supported by the data presented in the paper.