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DDX55 通过与 BRD4 相互作用并参与外泌体介导的细胞间通讯促进肝细胞癌进展。

DDX55 promotes hepatocellular carcinoma progression by interacting with BRD4 and participating in exosome-mediated cell-cell communication.

机构信息

Zhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, National Quality Control Center for Donated Organ Procurement, Hubei Key Laboratory of Medical Technology on Transplantation, Hubei Clinical Research Center for Natural Polymer Biological Liver, Hubei Engineering Center of Natural Polymer-based Medical Materials, Wuhan, China.

出版信息

Cancer Sci. 2022 Sep;113(9):3002-3017. doi: 10.1111/cas.15393. Epub 2022 Jun 10.

DOI:10.1111/cas.15393
PMID:35514200
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9459289/
Abstract

The involvement of DEAD-box helicase 55 (DDX55) in oncogenesis has been suggested, but its biological role in hepatocellular carcinoma (HCC) remains unknown. The present study verified the upregulation of DDX55 in HCC tissues compared with non-tumor controls. DDX55 displayed the highest prognostic values among the DEAD-box protein family for recurrence-free survival and overall survival of HCC patients. In addition, the effects of DDX55 in the promotion of HCC cell proliferation, migration, and invasion were determined ex vivo and in vivo. Mechanistically, we revealed that DDX55 could interact with BRD4 to form a transcriptional regulatory complex that positively regulated PIK3CA transcription. Following that, β-catenin signaling was activated in a PI3K/Akt/GSK-3β dependent manner, thus inducing cell cycle progression and epithelial-mesenchymal transition. Intriguingly, both DDX55 mRNA and protein were identified in the exosomes derived from HCC cells. Exosomal DDX55 was implicated in intercellular communication between HCC cells with high or low DDX55 levels and between HCC cells and endothelial cells, thereby promoting the malignant phenotype of HCC cells and angiogenesis. In conclusion, DDX55 may be a valuable prognostic biomarker and therapeutic target in HCC.

摘要

DDX55 在肿瘤发生中的作用已被提出，但它在肝细胞癌 (HCC) 中的生物学作用尚不清楚。本研究证实 DDX55 在 HCC 组织中的表达高于非肿瘤对照。在 HCC 患者的无复发生存和总生存中，DDX55 在 DEAD-box 蛋白家族中具有最高的预后价值。此外，还在体外表征和体内确定了 DDX55 在促进 HCC 细胞增殖、迁移和侵袭中的作用。在机制上，我们揭示 DDX55 可以与 BRD4 相互作用形成转录调节复合物，从而正向调节 PIK3CA 转录。随后，β-连环蛋白信号通过 PI3K/Akt/GSK-3β 依赖性方式被激活，从而诱导细胞周期进程和上皮间质转化。有趣的是，在源自 HCC 细胞的外泌体中均鉴定出 DDX55 的 mRNA 和蛋白。外泌体 DDX55 参与高或低 DDX55 水平的 HCC 细胞之间以及 HCC 细胞与内皮细胞之间的细胞间通讯，从而促进 HCC 细胞的恶性表型和血管生成。总之，DDX55 可能是 HCC 中有价值的预后生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d92/9459289/fbbef0ab7631/CAS-113-3002-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d92/9459289/fbbef0ab7631/CAS-113-3002-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d92/9459289/839ef506147e/CAS-113-3002-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d92/9459289/b29e702a0cdf/CAS-113-3002-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d92/9459289/fe3c45ab8cd7/CAS-113-3002-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d92/9459289/97d66b34c2d2/CAS-113-3002-g005.jpg
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