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FAM84B通过网络改变促进前列腺肿瘤发生。

FAM84B promotes prostate tumorigenesis through a network alteration.

作者信息

Jiang Yanzhi, Lin Xiaozeng, Kapoor Anil, He Lizhi, Wei Fengxiang, Gu Yan, Mei Wenjuan, Zhao Kuncheng, Yang Huixiang, Tang Damu

机构信息

Department of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, China Department of Medicine, McMaster University, Hamilton, ON, Canada Father Sean O'Sullivan Research Institute, St. Joseph's Hospital, Hamilton, ON. Canada Hamilton Center for Kidney Research, St. Joseph's Hospital, Hamilton, ON, Canada Hamilton Urologic Urological Cancer Center for Research and Innovation (UCCRI), St. Joseph's Hospital, Hamilton, ON, Canada.

Department of Medicine, McMaster University, Hamilton, ON, Canada Father Sean O'Sullivan Research Institute, St. Joseph's Hospital/Hamilton Center for Kidney Research, St. Joseph's Hospital, Hamilton, ON, Canada Urological Cancer Center for Research and Innovation (UCCRI), St. Joseph's Hospital, Hamilton, ON, Canada.

出版信息

Ther Adv Med Oncol. 2019 May 13;11:1758835919846372. doi: 10.1177/1758835919846372. eCollection 2019.

DOI:10.1177/1758835919846372
PMID:
31205500
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6535720/
Abstract

BACKGROUND

The aim of this study was to investigate the contributions of FAM84B in prostate tumorigenesis and progression.

METHODS

A FAM84B mutant with deletion of its HRASLS domain (ΔHRASLS) was constructed. DU145 prostate cancer (PC) cells stably expressing an empty vector (EV), FAM84B, or FAM84B (ΔHRASLS) were produced. These lines were examined for proliferation, invasion, and growth in soft agar DU145 EV and FAM84B cells were investigated for tumor growth and lung metastasis in NOD/SCID mice. The transcriptome of DU145 EV xenografts ( = 2) and DU145 FAM84B tumors ( = 2) was determined using RNA sequencing, and analyzed for pathway alterations. The FAM84B-affected network was evaluated for an association with PC recurrence.

RESULTS

FAM84B but not FAM84B (ΔHRASLS) increased DU145 cell invasion and growth in soft agar. Co-immunoprecipitation and co-localization analyses revealed an interaction between FAM84B and FAM84B (ΔHRASLS), suggesting an intramolecular association among FAM84B molecules. FAM84B significantly enhanced DU145 cell-derived xenografts and lung metastasis. In comparison with DU145 EV cell-produced tumors, those generated by DU145 FAM84B cells showed a large number of differentially expressed genes (DEGs; = 4976). A total of 51 pathways were enriched in these DEGs, which function in the Golgi-to-endoplasmic reticulum processes, cell cycle checkpoints, mitochondrial events, and protein translation. A novel 27-gene signature (SigFAM) was derived from these DEGs; SigFAM robustly stratifies PC recurrence in two large PC populations ( = 490, = 0; = 140, = 4e), and remains an independent risk factor of PC recurrence after adjusting for age at diagnosis, Gleason scores, surgical margin, and tumor stages.

CONCLUSIONS

FAM84B promotes prostate tumorigenesis through a complex network that predicts PC recurrence.

摘要

背景

本研究旨在探究FAM84B在前列腺癌发生和进展中的作用。

方法

构建了缺失HRASLS结构域（ΔHRASLS）的FAM84B突变体。制备了稳定表达空载体（EV）、FAM84B或FAM84B（ΔHRASLS）的DU145前列腺癌细胞系。检测这些细胞系在软琼脂中的增殖、侵袭和生长情况。对DU145 EV和FAM84B细胞在NOD/SCID小鼠体内的肿瘤生长和肺转移情况进行研究。使用RNA测序确定DU145 EV异种移植瘤（n = 2）和DU145 FAM84B肿瘤（n = 2）的转录组，并分析其通路改变。评估受FAM84B影响的网络与前列腺癌复发的相关性。

结果

FAM84B而非FAM84B（ΔHRASLS）增加了DU145细胞在软琼脂中的侵袭和生长。免疫共沉淀和共定位分析揭示了FAM84B与FAM84B（ΔHRASLS）之间的相互作用，提示FAM84B分子间存在分子内关联。FAM84B显著增强了DU145细胞来源的异种移植瘤生长和肺转移。与DU145 EV细胞产生的肿瘤相比，DU145 FAM84B细胞产生的肿瘤显示出大量差异表达基因（DEGs；n = 4976）。这些DEGs共富集了51条通路，其功能涉及高尔基体到内质网过程、细胞周期检查点、线粒体事件和蛋白质翻译。从这些DEGs中得出一个新的27基因特征（SigFAM）；SigFAM在两个大型前列腺癌群体中（n = 490，P = 0；n = 140，P = 4e）能有力地分层前列腺癌复发情况，并且在调整诊断年龄、Gleason评分、手术切缘和肿瘤分期后，仍然是前列腺癌复发的独立危险因素。

结论

FAM84B通过一个预测前列腺癌复发的复杂网络促进前列腺癌发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/2f2e1863c5a8/10.1177_1758835919846372-fig13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/5b806aa77160/10.1177_1758835919846372-fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/111453a98c38/10.1177_1758835919846372-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/731ef8dfcb23/10.1177_1758835919846372-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/79965b4aa98e/10.1177_1758835919846372-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/cb3e050c7b95/10.1177_1758835919846372-fig11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/927ad888237d/10.1177_1758835919846372-fig12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/2f2e1863c5a8/10.1177_1758835919846372-fig13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/5b806aa77160/10.1177_1758835919846372-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/eb59b8a0b930/10.1177_1758835919846372-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/0aa457040f4f/10.1177_1758835919846372-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/372ae7385cbc/10.1177_1758835919846372-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/e97c4f2028f9/10.1177_1758835919846372-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/fe008b3b4d90/10.1177_1758835919846372-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/7b70c14fc02c/10.1177_1758835919846372-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/111453a98c38/10.1177_1758835919846372-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/731ef8dfcb23/10.1177_1758835919846372-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/79965b4aa98e/10.1177_1758835919846372-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/cb3e050c7b95/10.1177_1758835919846372-fig11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/927ad888237d/10.1177_1758835919846372-fig12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313d/6535720/2f2e1863c5a8/10.1177_1758835919846372-fig13.jpg

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