Role of the HGF/c-MET tyrosine kinase inhibitors in metastasic melanoma

被引:0
|
作者
Lucia Demkova
Lucia Kucerova
机构
[1] Biomedical Research Center of the Slovak Academy of Sciences,Laboratory of Molecular Oncology, Cancer Research Institute
来源
关键词
Metastasis; Malignant melanoma; Hepatocyte growth factor; C-met receptor; Tyrosine kinase inhibitors; A375 Human malignant melanoma cell line.;
D O I
暂无
中图分类号
学科分类号
摘要
Metastatic disease in a cancer patient still remains a therapeutic challenge. Metastatic process involves many steps, during which malignant cells succeed to activate cellular pathways promoting survival in hostile environment, engraftment and growth at the distant site from the primary tumor. Melanoma is known for its high propensity to produce metastases even at the early stages of the disease. Here we summarize the most important molecular mechanisms which were associated with the melanoma metastasis. Then, we specifically focus on the signaling pathway mediated by hepatocyte growth factor (HGF) and its receptor c-Met, which play an important role during physiological processes and were been associated with tumorigenesis. We also focus on the effect of the small molecule inhibitors of the tyrosine kinase domain of the c-Met receptor and its effects on properties of melanoma cell. We summarize recent studies, which involved inhibition of the HGF/c-Met signaling in order to decrease melanoma growth and metastatic capacity.
引用
收藏
相关论文
共 50 条
  • [21] The role of SF/HGF and c-Met in the development of skeletal muscle
    Dietrich, S
    Abou-Rebyeh, F
    Brohmann, H
    Bladt, F
    Sonnenberg-Riethmacher, E
    Yamaai, T
    Lumsden, A
    Brand-Saberi, B
    Birchmeier, C
    DEVELOPMENT, 1999, 126 (08): : 1621 - 1629
  • [22] A role for lactate dehydrogenase in the c-Met/HGF signaling axis
    Gray, Alana L.
    Minutolo, Filippo
    Cardelli, James A.
    CANCER RESEARCH, 2012, 72
  • [23] Identification of the receptor tyrosine kinase c-Met and its ligand, HGF, as therapeutic targets in clear cell sarcoma
    Davis, I.
    Coxon, A.
    Goldberg, J.
    Burgess, T.
    Fisher, D.
    EJC SUPPLEMENTS, 2006, 4 (12): : 187 - 187
  • [24] Lack of oncogenic mutations in the c-Met catalytic tyrosine kinase domain in acral lentiginous melanoma
    Seidl, Hannes
    Weger, Wolfgang
    Wolf, Peter
    Kerl, Helmut
    Schaider, Helmut
    INTERNATIONAL JOURNAL OF DERMATOLOGY, 2008, 47 (12) : 1327 - 1329
  • [25] Novel targets mediating resistance to EGFR/c-Met tyrosine kinase inhibitors in NSCLC.
    Jacobs, Ryan
    Fong, Jason
    Moravec, David
    Botting, Greg
    Bomgarden, Ryan
    Rogers, John
    Viner, Rosa
    Blank, Michael
    Puri, Neelu
    CANCER RESEARCH, 2013, 73 (08)
  • [26] Optimization techniques for novel c-Met kinase inhibitors
    Sun, Zhi-Gang
    Yang, Yong-An
    Zhang, Zhi-Gang
    Zhu, Hai-Liang
    EXPERT OPINION ON DRUG DISCOVERY, 2019, 14 (01) : 59 - 69
  • [27] Recent Patents on the Development of c-Met Kinase Inhibitors
    Xu, Xiangming
    Yao, Lei
    RECENT PATENTS ON ANTI-CANCER DRUG DISCOVERY, 2020, 15 (03) : 228 - 238
  • [28] Chemical inhibitors of c-Met receptor tyrosine kinase stimulate osteoblast differentiation and bone regeneration
    Kim, Jung-Woo
    Lee, Mi Nam
    Jeong, Byung-Chul
    Oh, Sin-Hye
    Kook, Min-Suk
    Koh, Jeong-Tae
    EUROPEAN JOURNAL OF PHARMACOLOGY, 2017, 806 : 10 - 17
  • [29] Quercetin inhibits HGF/c-Met signaling and HGF-stimulated melanoma cell migration and invasion
    Hui-Hui Cao
    Chi-Yan Cheng
    Tao Su
    Xiu-Qiong Fu
    Hui Guo
    Ting Li
    Anfernee Kai-Wing Tse
    Hiu-Yee Kwan
    Hua Yu
    Zhi-Ling Yu
    Molecular Cancer, 14
  • [30] HGF-MET in Resistance to EGFR Tyrosine Kinase Inhibitors in Lung Cancer
    Yano, Seiji
    Wang, Wei
    Li, Qi
    Yamada, Tadaaki
    Takeuchi, Shinji
    Matsumoto, Kunio
    Nishioka, Yasuhiko
    Sone, Saburo
    CURRENT SIGNAL TRANSDUCTION THERAPY, 2011, 6 (02) : 228 - 233