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表皮生长因子受体(EGFR)和间质上皮转化因子(MET)抑制剂的联合使用可降低黏膜黑色素瘤细胞的增殖和侵袭能力。

Combinations of EGFR and MET inhibitors reduce proliferation and invasiveness of mucosal melanoma cells.

作者信息

Simiczyjew Aleksandra, Wądzyńska Justyna, Kot Magdalena, Ziętek Marcin, Matkowski Rafał, Hoang Mai P, Donizy Piotr, Nowak Dorota

机构信息

Department of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, Wroclaw, Poland.

Department of Oncology and Division of Surgical Oncology, Wroclaw Medical University, Wroclaw, Poland.

出版信息

J Cell Mol Med. 2023 Oct;27(19):2995-3008. doi: 10.1111/jcmm.17935. Epub 2023 Sep 7.

DOI:10.1111/jcmm.17935
PMID:37679999
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10538264/
Abstract

Mucosal melanoma (MM) is a very rare and aggressive type of cancer for which immunotherapy or targeted therapy such as BRAF/MEK inhibitors, used in cutaneous melanoma, usually fail. Due to our earlier experience showing the high effectiveness of epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (MET) inhibitors in reducing the activation of the MAPK and PI3K/AKT signalling pathways, we aim to test whether these drugs would also be effective for mucosal melanoma. Cells representing two commercially available mucosal melanoma cell lines (GAK and HMVII) and one cell line obtained from a patient's vaginal melanoma were treated with MET or EGFR inhibitors, or combinations of these agents. The dual-inhibitor treatment strategy resulted in a decrease of cell proliferation, migration and invasion. Moreover, combinations of inhibitors led to reduction of pEGFR/EGFR and pMET/MET ratio and downregulation of PI3K/AKT and MEK/ERK1/2-based signalling pathways. Our findings indicate a potential therapeutic strategy based on EGFR and MET inhibitors in mucosal melanoma, which should be further evaluated in vivo and in clinical experiments. They also suggest that targeting multiple receptor tyrosine kinases may block signalling crosstalk and possibly delay the appearance of resistance to kinase inhibitors in mucosal melanoma cells.

摘要

黏膜黑色素瘤(MM)是一种非常罕见且侵袭性强的癌症类型,用于皮肤黑色素瘤的免疫疗法或靶向疗法(如BRAF/MEK抑制剂)通常对其无效。鉴于我们早期的经验表明表皮生长因子受体(EGFR)和肝细胞生长因子受体(MET)抑制剂在降低MAPK和PI3K/AKT信号通路激活方面具有高效性,我们旨在测试这些药物对黏膜黑色素瘤是否也有效。用MET或EGFR抑制剂或这些药物的组合处理代表两种市售黏膜黑色素瘤细胞系(GAK和HMVII)以及一种从患者阴道黑色素瘤获得的细胞系的细胞。双重抑制剂治疗策略导致细胞增殖、迁移和侵袭减少。此外,抑制剂组合导致pEGFR/EGFR和pMET/MET比值降低以及基于PI3K/AKT和MEK/ERK1/2的信号通路下调。我们的研究结果表明基于EGFR和MET抑制剂的黏膜黑色素瘤潜在治疗策略,应在体内和临床试验中进一步评估。它们还表明靶向多种受体酪氨酸激酶可能会阻断信号串扰,并可能延迟黏膜黑色素瘤细胞对激酶抑制剂耐药性的出现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/44faaaaebd1a/JCMM-27-2995-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/b14e80005062/JCMM-27-2995-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/d293a6467e08/JCMM-27-2995-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/9106eaf567aa/JCMM-27-2995-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/4f239a8e47d3/JCMM-27-2995-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/dd9f26727fd8/JCMM-27-2995-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/daa59d6847b4/JCMM-27-2995-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/44faaaaebd1a/JCMM-27-2995-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/b14e80005062/JCMM-27-2995-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/d293a6467e08/JCMM-27-2995-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/9106eaf567aa/JCMM-27-2995-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/4f239a8e47d3/JCMM-27-2995-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/dd9f26727fd8/JCMM-27-2995-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/daa59d6847b4/JCMM-27-2995-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d69/10538264/44faaaaebd1a/JCMM-27-2995-g003.jpg

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