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NOP14通过调节Wnt/β-连环蛋白信号通路抑制黑色素瘤的增殖和转移。

NOP14 inhibits melanoma proliferation and metastasis by regulating Wnt/β-catenin signaling pathway.

作者信息

Li Jingrong, Fang Ruihua, Wang Jianqin, Deng Liehua

机构信息

Department of Dermatology, The First Affiliated Hospital of Jinan University, Guangzhou, China.

Department of Dermatology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.

出版信息

Braz J Med Biol Res. 2018 Nov 23;52(1):e7952. doi: 10.1590/1414-431X20187952.

DOI:10.1590/1414-431X20187952
PMID:30484495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6262753/
Abstract

Malignant melanoma is an aggressive skin cancer with a high mortality rate. Nucleolar protein 14 (NOP14) has been implicated in cancer development. However, the role of NOP14 in malignant melanoma progression remains largely unclear. In this study, we observed that malignant melanoma tissue showed NOP14 down-regulation compared to melanocytic nevi tissues. Moreover, we observed that NOP14 expression was significantly associated with melanoma tumor thickness and lymph node metastasis. NOP14 overexpression in melanoma cells suppressed proliferation, caused G1 phase arrest, promoted apoptosis, and inhibited melanoma cell migration and invasion. Further investigations revealed that NOP14 overexpression reduced the expression levels of Wnt3a, β-catenin, and GSK-3β of the Wnt/β-catenin pathway. In summary, we demonstrated that NOP14 inhibited melanoma cell proliferation and metastasis by regulating the Wnt/β-catenin signaling pathway.

摘要

恶性黑色素瘤是一种侵袭性皮肤癌,死亡率很高。核仁蛋白14(NOP14)与癌症发展有关。然而,NOP14在恶性黑色素瘤进展中的作用仍不清楚。在本研究中,我们观察到与黑素细胞痣组织相比,恶性黑色素瘤组织中NOP14表达下调。此外,我们观察到NOP14表达与黑色素瘤肿瘤厚度和淋巴结转移显著相关。黑色素瘤细胞中NOP14过表达抑制增殖,导致G1期阻滞,促进凋亡,并抑制黑色素瘤细胞迁移和侵袭。进一步研究表明,NOP14过表达降低了Wnt/β-连环蛋白通路中Wnt3a、β-连环蛋白和GSK-3β的表达水平。总之,我们证明NOP14通过调节Wnt/β-连环蛋白信号通路抑制黑色素瘤细胞增殖和转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/c61a1cfe645f/1414-431X-bjmbr-52-1-e7952-gf005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/19aadbb12f97/1414-431X-bjmbr-52-1-e7952-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/41d6aea8928f/1414-431X-bjmbr-52-1-e7952-gf002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/0a67276e9646/1414-431X-bjmbr-52-1-e7952-gf003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/15381eef3126/1414-431X-bjmbr-52-1-e7952-gf004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/c61a1cfe645f/1414-431X-bjmbr-52-1-e7952-gf005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/19aadbb12f97/1414-431X-bjmbr-52-1-e7952-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/41d6aea8928f/1414-431X-bjmbr-52-1-e7952-gf002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/0a67276e9646/1414-431X-bjmbr-52-1-e7952-gf003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/15381eef3126/1414-431X-bjmbr-52-1-e7952-gf004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a609/6262753/c61a1cfe645f/1414-431X-bjmbr-52-1-e7952-gf005.jpg

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