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多西他赛联合安维汀治疗在晚期前列腺癌患者来源异种移植模型中可显著抑制转移。

Treatment with docetaxel in combination with Aneustat leads to potent inhibition of metastasis in a patient-derived xenograft model of advanced prostate cancer.

机构信息

Department of Experimental Therapeutics, BC Cancer Agency, Vancouver, BC V5Z 1L3 Canada.

Vancouver Prostate Centre, Vancouver, BC V6H 3Z6, Canada.

出版信息

Br J Cancer. 2018 Mar 20;118(6):802-812. doi: 10.1038/bjc.2017.474. Epub 2018 Jan 30.

DOI:10.1038/bjc.2017.474
PMID:29381682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5877435/
Abstract

BACKGROUND

Docetaxel used for first-line treatment of advanced prostate cancer (PCa) is only marginally effective. We previously showed, using the LTL-313H subrenal capsule patient-derived metastatic PCa xenograft model, that docetaxel combined with Aneustat (OMN54), a multivalent plant-derived therapeutic, led to marked synergistic tumour growth inhibition. Here, we investigated the effect of docetaxel+Aneustat on metastasis.

METHODS

C4-2 cells were incubated with docetaxel, Aneustat and docetaxel+Aneustat to assess effects on cell migration. The LTL-313H model, similarly treated, was analysed for effects on lung micro-metastasis and kidney invasion. The LTL-313H gene expression profile was compared with profiles of PCa patients (obtained from Oncomine) and subjected to IPA to determine involvement of cancer driver genes.

RESULTS

Docetaxel+Aneustat markedly inhibited C4-2 cell migration and LTL-313H lung micro-metastasis/kidney invasion. Oncomine analysis indicated that treatment with docetaxel+Aneustat was associated with improved patient outcome. The drug combination markedly downregulated expression of cancer driver genes such as FOXM1 (and FOXM1-target genes). FOXM1 overexpression reduced the anti-metastatic activity of docetaxel+Aneustat.

CONCLUSIONS

Docetaxel+Aneustat can inhibit PCa tissue invasion and metastasis. This activity appears to be based on reduced expression of cancer driver genes such as FOXM1. Use of docetaxel+Aneustat may provide a new, more effective regimen for therapy of metastatic PCa.

摘要

背景

多西紫杉醇用于治疗晚期前列腺癌（PCa）的一线治疗效果仅略有改善。我们之前使用 LTL-313H 肾包膜下患者来源的转移性 PCa 异种移植模型表明，多西紫杉醇联合 Aneustat（OMN54），一种多价植物衍生治疗药物，导致明显的协同肿瘤生长抑制作用。在这里，我们研究了多西紫杉醇+Aneustat 对转移的影响。

方法

将 C4-2 细胞与多西紫杉醇、Aneustat 和多西紫杉醇+Aneustat 孵育，以评估对细胞迁移的影响。同样处理的 LTL-313H 模型被分析用于肺微转移和肾脏侵袭的影响。将 LTL-313H 的基因表达谱与 PCa 患者的（从 Oncomine 获得）进行比较，并进行 IPA 分析以确定癌症驱动基因的参与。

结果

多西紫杉醇+Aneustat 显著抑制 C4-2 细胞迁移和 LTL-313H 肺微转移/肾脏侵袭。Oncomine 分析表明，多西紫杉醇+Aneustat 治疗与改善患者预后相关。药物联合显著下调了 FOXM1（和 FOXM1 靶基因）等癌症驱动基因的表达。FOXM1 过表达降低了多西紫杉醇+Aneustat 的抗转移活性。

结论

多西紫杉醇+Aneustat 可抑制 PCa 组织侵袭和转移。这种活性似乎基于降低癌症驱动基因（如 FOXM1）的表达。使用多西紫杉醇+Aneustat 可能为转移性 PCa 的治疗提供一种新的、更有效的方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/ed93055a09ad/bjc2017474f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/cd8c487d64ea/bjc2017474f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/38bcec105971/bjc2017474f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/c3e9305eb182/bjc2017474f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/fd162a16ea14/bjc2017474f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/ed93055a09ad/bjc2017474f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/cd8c487d64ea/bjc2017474f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/38bcec105971/bjc2017474f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/c3e9305eb182/bjc2017474f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/fd162a16ea14/bjc2017474f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c68b/5877435/ed93055a09ad/bjc2017474f5.jpg

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