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DDX54通过激活结直肠癌中的P65和AKT信号通路发挥致癌作用。

DDX54 Plays a Cancerous Role Through Activating P65 and AKT Signaling Pathway in Colorectal Cancer.

作者信息

Yu Yi, Wang Jing-Long, Meng Li-Li, Hu Chun-Ting, Yan Zhao-Wen, He Zhi-Ping, Shi Xiao-Qin, Fu Guo-Hui, Zu Li-Dong

机构信息

Pathology Center, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.

Department of Pathology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

Front Oncol. 2021 Apr 21;11:650360. doi: 10.3389/fonc.2021.650360. eCollection 2021.

DOI:10.3389/fonc.2021.650360
PMID:33968751
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8097168/
Abstract

Colorectal cancer (CRC) is one of the most malignant cancers, and its incidence is still steadily increasing. The DDX RNA helicase family members have been found to play a role in various cancers; however, the role of DDX54 in colorectal cancer is still unclear and needed to be defined. Here, we found DDX54 was overexpressed in CRC tissues by the label-free mass spectrum, which was also verified in tissue microarray of colon cancer, as well as the CRC cell lines and TCGA database. High DDX54 level was correlated with tumor stage and distant metastasis, which always indicated a poor prognosis to the CRC patients. DDX54 could promote the proliferation and mobility of CRC cells through increasing the phosphorylation level p65 and AKT leading to the tumorigenesis. Here, we have preliminarily studied the function of DDX54 in CRC, which would improve our understanding of the underlying biology of CRC and provide the new insight that could be translated into novel therapeutic approaches.

摘要

结直肠癌(CRC)是最具恶性的癌症之一,其发病率仍在稳步上升。已发现DDX RNA解旋酶家族成员在多种癌症中发挥作用;然而,DDX54在结直肠癌中的作用仍不清楚,需要进一步明确。在此,我们通过无标记质谱法发现DDX54在CRC组织中过表达,这在结肠癌组织芯片、CRC细胞系和TCGA数据库中也得到了验证。高DDX54水平与肿瘤分期和远处转移相关,这通常表明CRC患者预后不良。DDX54可通过增加p65和AKT的磷酸化水平促进CRC细胞的增殖和迁移,从而导致肿瘤发生。在此,我们初步研究了DDX54在CRC中的功能,这将增进我们对CRC潜在生物学特性的理解,并提供可转化为新型治疗方法的新见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/8419e25ae7de/fonc-11-650360-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/ca108c4702bc/fonc-11-650360-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/b7623867da71/fonc-11-650360-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/02ecc06c0619/fonc-11-650360-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/f83e47c2c968/fonc-11-650360-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/c0bbcdbed768/fonc-11-650360-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/8419e25ae7de/fonc-11-650360-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/ca108c4702bc/fonc-11-650360-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/b7623867da71/fonc-11-650360-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/02ecc06c0619/fonc-11-650360-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/f83e47c2c968/fonc-11-650360-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/c0bbcdbed768/fonc-11-650360-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89e/8097168/8419e25ae7de/fonc-11-650360-g006.jpg

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