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CLEC4D作为一种新型预后标志物，通过NF-κB/AKT信号通路促进胃癌的增殖和迁移。

CLEC4D as a Novel Prognostic Marker Boosts the Proliferation and Migration of Gastric Cancer via the NF-κB/AKT Signaling Pathway.

作者信息

Yang Yang, Zhang Mengmeng, Cai Fenglin, Ma Gang, Zhang Ru-Peng, Yin Yiqing, Deng Jingyu

机构信息

Department of Gastric Surgery, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, People's Republic of China.

Department of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, 300060, People's Republic of China.

出版信息

Int J Gen Med. 2024 May 6;17:1923-1935. doi: 10.2147/IJGM.S458228. eCollection 2024.

DOI:10.2147/IJGM.S458228
PMID:38736669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11088047/
Abstract

PURPOSE

The functions of C-type lectin domain family 4 member D (CLEC4D), one member of the C-type lectin/C-type lectin-like domain superfamily, in immunity have been well described, but its roles in cancer biology remain largely unknown.

PATIENTS AND METHODS

This study aims to explore the role of CLEC4D in gastric cancer (GC). Bioinformatics preliminarily analyzed the expression of CLEC4D in gastric cancer. Immunohistochemical staining was used to detect the expression level and clinical pathological characteristics of CLEC4D in gastric cancer. The biological function of CLEC4D in gastric cancer cell lines was verified through in vitro and in vivo experiments.

RESULTS

In this study, CLEC4D expression was found to be markedly increased in gastric cancer (GC) tissues compared with matched normal gastric tissues, and high CLEC4D expression independently predicted unfavorable overall survival in patients with GC. Knockdown of CLEC4D markedly inhibited GC cell proliferation and migration. Mechanistically, CLEC4D knockdown deactivated the Akt and NF-κB signaling pathways in GC cells.

CONCLUSION

Together, these results demonstrate that aberrantly increased CLEC4D expression promotes cancer phenotypes via the Akt and NF-κB signaling pathways in GC cells.

摘要

目的

C型凝集素结构域家族4成员D（CLEC4D）是C型凝集素/C型凝集素样结构域超家族的一员，其在免疫中的功能已得到充分描述，但其在癌症生物学中的作用仍 largely unknown。

患者与方法

本研究旨在探讨CLEC4D在胃癌（GC）中的作用。生物信息学初步分析了CLEC4D在胃癌中的表达。采用免疫组织化学染色检测CLEC4D在胃癌中的表达水平及临床病理特征。通过体外和体内实验验证CLEC4D在胃癌细胞系中的生物学功能。

结果

在本研究中，发现与配对的正常胃组织相比，胃癌（GC）组织中CLEC4D表达明显增加，且高CLEC4D表达独立预测GC患者的总体生存不良。敲低CLEC4D可显著抑制GC细胞增殖和迁移。机制上，敲低CLEC4D可使GC细胞中的Akt和NF-κB信号通路失活。

结论

总之，这些结果表明，异常增加的CLEC4D表达通过GC细胞中的Akt和NF-κB信号通路促进癌症表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/d11fc9d40840/IJGM-17-1923-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/cb8529bcc1c5/IJGM-17-1923-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/7af3495218ce/IJGM-17-1923-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/368e4b37aec3/IJGM-17-1923-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/d11fc9d40840/IJGM-17-1923-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/cb8529bcc1c5/IJGM-17-1923-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/7af3495218ce/IJGM-17-1923-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/368e4b37aec3/IJGM-17-1923-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d48/11088047/d11fc9d40840/IJGM-17-1923-g0004.jpg

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