Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development

التفاصيل البيبلوغرافية
العنوان: Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development
المؤلفون: Escarlet Díaz-Galicia, Stefan T. Arold, Rayan Naser, Abdullah Aldehaiman
المصدر: Cancers, Vol 10, Iss 6, p 196 (2018)
Cancers
بيانات النشر: MDPI AG, 2018.
سنة النشر: 2018
مصطلحات موضوعية: 0301 basic medicine, Cancer Research, PTEN, LKB1, chaperon, Review, Biology, PI3K, lcsh:RC254-282, Metastasis, Focal adhesion, 03 medical and health sciences, 0302 clinical medicine, anoikis, microRNA, medicine, Anoikis, FIP200, PI3K/AKT/mTOR pathway, miRNA, dimerization, Kinase, regulation, medicine.disease, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, 030104 developmental biology, Oncology, motility, Tyrosine kinase 2, 030220 oncology & carcinogenesis, Cancer cell, Cancer research
الوصف: Focal adhesion kinase (FAK) and its close paralogue, proline-rich tyrosine kinase 2 (PYK2), are key regulators of aggressive spreading and metastasis of cancer cells. While targeted small-molecule inhibitors of FAK and PYK2 have been found to have promising antitumor activity, their clinical long-term efficacy may be undermined by the strong capacity of cancer cells to evade anti-kinase drugs. In healthy cells, the expression and/or function of FAK and PYK2 is tightly controlled via modulation of gene expression, competing alternatively spliced forms, non-coding RNAs, and proteins that directly or indirectly affect kinase activation or protein stability. The molecular factors involved in this control are frequently deregulated in cancer cells. Here, we review the endogenous mechanisms controlling FAK and PYK2, and with particular focus on how these mechanisms could inspire or improve anticancer therapies.
اللغة: English
تدمد: 2072-6694
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::023ed276c663adc9873730b2671f5f92
http://www.mdpi.com/2072-6694/10/6/196
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....023ed276c663adc9873730b2671f5f92
قاعدة البيانات: OpenAIRE