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研究膜相关环-CH 型手指蛋白 9 在结直肠癌中的预后和致癌作用。

Investigating the Prognostic and Oncogenic Roles of Membrane-Associated Ring-CH-Type Finger 9 in Colorectal Cancer.

机构信息

Department of Gynecology The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Department of Nuclear Medicine The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

出版信息

Genet Res (Camb). 2024 Aug 17;2024:9279653. doi: 10.1155/2024/9279653. eCollection 2024.

DOI:10.1155/2024/9279653
PMID:39185021
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11344643/
Abstract

. Colorectal cancer (CRC) represents a major global health challenge, necessitating comprehensive investigations into its underlying molecular mechanisms to enhance diagnostic and therapeutic strategies. This study focuses on elucidating the oncogenic role of Membrane-Associated Ring-CH-Type Finger 9 (MARCHF9), a RING-Type E3 ubiquitin transferase, in CRC. We aim to assess MARCHF9's clinical significance, functional impact on CRC progression, and its potential as a prognostic biomarker. . We leveraged data from the Cancer Genome Atlas (TCGA) cohort to evaluate MARCHF9 expression profiles in CRC. In vitro experiments involved siRNA-mediated MARCHF9 knockdown in COAD cell lines (SW480 and LoVo). Cell proliferation and invasion assays were conducted to investigate MARCHF9's functional relevance. Survival analyses were performed to assess its prognostic role. . Our analysis revealed significantly elevated MARCHF9 expression in CRC tissues compared to normal colorectal tissues ( < 0.05). High MARCHF9 expression correlated with advanced clinical stages, distant metastases, and the presence of residual tumors in CRC patients. Survival analyses demonstrated that high MARCHF9 expression predicted unfavorable overall and disease-free survival outcomes ( < 0.05). In vitro experiments further supported its oncogenic potential, with MARCHF9 knockdown inhibiting COAD cell proliferation and invasion. . This study unveils the oncogenic role of MARCHF9 in CRC, highlighting its clinical relevance as a potential biomarker and therapeutic target. MARCHF9's association with adverse clinicopathological features and its functional impact on cancer cell behavior underscore its significance in CRC progression. Further research is essential to elucidate precise mechanisms by which MARCHF9 enhances tumorigenesis and to explore its therapeutic potential in CRC management.

摘要

. 结直肠癌(CRC)是一个全球性的重大健康挑战,需要对其潜在的分子机制进行全面研究,以增强诊断和治疗策略。本研究旨在阐明膜相关环-CH 型手指 9(MARCHF9)作为一种 RING 型 E3 泛素转移酶在 CRC 中的致癌作用。我们旨在评估 MARCHF9 的临床意义、对 CRC 进展的功能影响及其作为预后生物标志物的潜力。. 我们利用癌症基因组图谱(TCGA)队列的数据评估了 CRC 中 MARCHF9 的表达谱。在体外实验中,我们使用 siRNA 介导的 COAD 细胞系(SW480 和 LoVo)中的 MARCHF9 敲低。进行细胞增殖和侵袭实验以研究 MARCHF9 的功能相关性。进行生存分析以评估其预后作用。. 我们的分析显示,CRC 组织中的 MARCHF9 表达明显高于正常结直肠组织(<0.05)。高 MARCHF9 表达与 CRC 患者的晚期临床分期、远处转移和残留肿瘤有关。生存分析表明,高 MARCHF9 表达预示着不利的总生存期和无病生存期结局(<0.05)。体外实验进一步支持了其致癌潜能,MARCHF9 敲低抑制了 COAD 细胞的增殖和侵袭。. 本研究揭示了 MARCHF9 在 CRC 中的致癌作用,强调了其作为潜在生物标志物和治疗靶点的临床相关性。MARCHF9 与不良临床病理特征的关联及其对癌细胞行为的功能影响突出了其在 CRC 进展中的重要性。进一步的研究对于阐明 MARCHF9 增强肿瘤发生的精确机制以及探索其在 CRC 管理中的治疗潜力至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/63da8fff5c66/GR2024-9279653.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/486cefe663e9/GR2024-9279653.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/b15ba6912a70/GR2024-9279653.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/cb5cdf96a912/GR2024-9279653.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/63da8fff5c66/GR2024-9279653.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/486cefe663e9/GR2024-9279653.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/b15ba6912a70/GR2024-9279653.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/cb5cdf96a912/GR2024-9279653.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b4/11344643/63da8fff5c66/GR2024-9279653.004.jpg

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The role of MARCH9 in colorectal cancer progression.
MARCH9在结直肠癌进展中的作用。
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PRDM5 suppresses oesophageal squamous carcinoma cells and modulates 14-3-3zeta/Akt signalling pathway.PRDM5 抑制食管鳞癌细胞并调节 14-3-3zeta/Akt 信号通路。
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EZH2 upregulates the expression of MAPK1 to promote intervertebral disc degeneration via suppression of miR-129-5p.EZH2通过抑制miR-129-5p上调MAPK1的表达以促进椎间盘退变。
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