FKBP۵۱ and Cancer Stem Cells: Coordinating Cancer Progression through the Molecular axis
- سال انتشار: 1403
- محل انتشار: دومین کنگره بین المللی کنسرژنومیکس
- کد COI اختصاصی: ICGCS02_211
- زبان مقاله: انگلیسی
- تعداد مشاهده: 129
نویسندگان
Department of Biology, Faculty of Sciences, Mashhad Branch, Islamic Azad University, Mashhad, Iran
Department of Medical Laboratory Sciences, Varastegan Institute for Medical Sciences, Mashhad, Iran
Department of Biology, Faculty of Sciences, Mashhad Branch, Islamic Azad University, Mashhad, Iran
چکیده
The significant role of FK۵۰۶-binding protein ۵۱ (FKBP۵۱) in the sustainment of cancer cell growth and aggressiveness in some human cancers. FKBP۵۱ has been related to several signaling pathways, tumorigenesis, chemoresistance and oncogenic processes. CSCs or CSC-like cells take part and are responsible for events in the pathogenesis of cancer, such as aggressive tumor progression, recurrent tumor growth, and spreading metastases. It has been reported that the role of FKBP۵۱ in modulating some of the primary pathways that regulate the survival and activity of CSCs: Wnt/β-catenin, NF-κB, and PI۳K/AKT. FKBP۵۱ leads the Wnt/β-catenin pathway and is essential for surviving and maintaining CSCs in breast cancer. Similarly, FKBP۵۱ participates in the NF-κB pathway and controls the growth and resistance to apoptosis of CSCs in prostate cancer. Increased stiffness activities of the YAP/TAZ pathway, enhancing the ability of CSCs for self-renewal and resistance to therapies. The interactions between matrix stiffness and the YAP/TAZ or other signaling pathways might reflect complex regulation for CSCs by FKBP۵۱.Furthermore, some new therapy strategies have been determined that existing drugs will be effective in targeting CSCs. Combinations with micronutrients could improve the anticancer properties and help reduce the side effects, which will be an innovative approach to overcoming CSC-mediated therapy resistance. Specific pathways such as Wnt, Hedgehog, and Notch are targeted in the chemoresistance of CSCs, and the inhibitors of these pathways show great potential in re-sensitizing CSCs and leading to the introduction of new and effective agents for cancer treatment. These pathways' inhibitors combined with conventional therapies could restore CSC sensitivity to treatments, determining new opportunities for effective cancer therapy.Furthermore,emerging evidence suggests that the role of FKBP۵۱ is beyond traditional signaling pathwayswhich may increase CSC survival and tumor growth. In conclusion, FKBP۵۱ coordinates cancer progression and metastasis by modulating CSC activities through multiple molecular transduction pathways.کلیدواژه ها
FK۵۰۶-binding protein ۵۱(FKBP۵۱), Cancer cell growth, Cancer stem cells (CSCs), Tumor microenvironment, therapy resistanceمقالات مرتبط جدید
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