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MUC1 过表达及其网络中的基因组改变与前列腺癌进展相关。

Overexpression of MUC1 and Genomic Alterations in Its Network Associate with Prostate Cancer Progression.

机构信息

Division of Nephrology, Department of Medicine, McMaster University; Father Sean O'Sullivan Research Institute; Hamilton Center for Kidney Research, St. Joseph's Hospital.

Father Sean O'Sullivan Research Institute; Department of Surgery, McMaster University, Hamilton, Ontario, Canada.

出版信息

Neoplasia. 2017 Nov;19(11):857-867. doi: 10.1016/j.neo.2017.06.006. Epub 2017 Sep 18.

DOI:10.1016/j.neo.2017.06.006
PMID:28930697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5605493/
Abstract

We investigate the association of MUC1 with castration-resistant prostate cancer (CRPC), bone metastasis, and PC recurrence. MUC1 expression was studied in patient-derived bone metastasis and CRPCs produced by prostate-specific PTEN mice and LNCaP xenografts. Elevations in MUC1 expression occur in CRPC. Among nine patients with hormone-naïve bone metastasis, eight express MUC1 in 61% to 100% of PC cells. Utilizing cBioPortal PC genomic data, we organized a training (n=300), testing (n=185), and validation (n=194) cohort. Using the Cox model, a nine-gene signature was derived, including eight genes from a MUC1-related network (APC, CTNNB1/β-catenin, GALNT10, GRB2, LYN, SIGLEC1, SOS1, and ZAP70) and FAM84B. Genomic alterations in these genes reduce disease-free survival (DFS) in the training (P=.00161), testing (P=.00699), entire (training+testing, P=5.557e-5), and a validation cohort (P=3.326e-5). The signature independently predicts PC recurrence [hazard ratio (HR)=1.731; 95% confidence interval (CI): 1.104-2.712; P=.0167] after adjusting for known clinical factors and stratifies patients with high risk of PC recurrence using the median (HR 2.072; 95% CI: 1.245-3.450, P=.0051) and quartile 3 (HR 3.707, 95% CI: 1.949-7.052, P=6.51e-5) scores. Several novel β-catenin mutants are identified in PCs leading to a rapid onset of death and recurrence. Genomic alterations in APC and CTNNB1/β-catenin reduce DFS in two independent PC cohorts (n=485, P=.0369; n=84, P=.0437). The nine-gene signature also associates with reductions in overall survival (P=.0458) and DFS (P=.0163) in melanoma patients (n=367). MUC1 upregulation is associated with CRPC and bone metastasis. A nine-gene signature derived from a MUC1 network predicts PC recurrence.

摘要

我们研究了 MUC1 与去势抵抗性前列腺癌（CRPC）、骨转移和 PC 复发的关联。在前列腺特异性 PTEN 小鼠和 LNCaP 异种移植产生的患者源性骨转移和 CRPC 中研究了 MUC1 的表达。在 CRPC 中，MUC1 的表达升高。在 9 名激素初治骨转移患者中，8 名患者有 61%至 100%的 PC 细胞表达 MUC1。利用 cBioPortal PC 基因组数据，我们组织了一个训练（n=300）、测试（n=185）和验证（n=194）队列。使用 Cox 模型，得出了一个由九个基因组成的特征，包括来自 MUC1 相关网络的八个基因（APC、CTNNB1/β-连环蛋白、GALNT10、GRB2、LYN、SIGLEC1、SOS1 和 ZAP70）和 FAM84B。这些基因的基因组改变降低了训练（P=.00161）、测试（P=.00699）、整个（训练+测试，P=5.557e-5）和验证队列（P=3.326e-5）中的无病生存期（DFS）。该特征独立预测 PC 复发[风险比（HR）=1.731；95%置信区间（CI）：1.104-2.712；P=.0167]，调整了已知的临床因素后，使用中位数（HR 2.072；95%CI：1.245-3.450，P=.0051）和四分位数 3（HR 3.707，95%CI：1.949-7.052，P=6.51e-5）评分对具有高 PC 复发风险的患者进行分层。在导致快速死亡和复发的 PCs 中鉴定出几种新型β-连环蛋白突变体。APC 和 CTNNB1/β-连环蛋白中的基因组改变降低了两个独立的 PC 队列（n=485，P=.0369；n=84，P=.0437）中的 DFS。九个基因特征也与黑色素瘤患者的总生存期（P=.0458）和 DFS（P=.0163）降低相关（n=367）。MUC1 的上调与 CRPC 和骨转移有关。源自 MUC1 网络的九个基因特征预测 PC 复发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/79b16e7313c9/gr14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/cdd5a352e06e/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/bb04e3c35859/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/fe49a42ef91c/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/df263ba4cb22/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/b6e68c0deafc/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/55dbbdde0bc1/gr12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/4167d7ad74a4/gr13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/79b16e7313c9/gr14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/cdd5a352e06e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/330d2ef7c2e4/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/5496790135eb/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/c6193b8e428a/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/2041bd788cb2/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/ee44715680f8/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/4b581f62d3d2/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/bb04e3c35859/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/fe49a42ef91c/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/df263ba4cb22/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/b6e68c0deafc/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/55dbbdde0bc1/gr12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/4167d7ad74a4/gr13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae79/5605493/79b16e7313c9/gr14.jpg

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