PTPN18 promotes colorectal cancer progression by regulating the c-MYC-CDK4 axis

التفاصيل البيبلوغرافية
العنوان: PTPN18 promotes colorectal cancer progression by regulating the c-MYC-CDK4 axis
المؤلفون: Xi-Cheng Huang, Xue-Min Song, Shang-Ze Li, Run-Lei Du, Jie Chen, Xiao-Dong Zhang, Wenbin Liu, Li Chao
المصدر: Genes & Diseases
Genes and Diseases, Vol 8, Iss 6, Pp 838-848 (2021)
بيانات النشر: Elsevier BV, 2021.
سنة النشر: 2021
مصطلحات موضوعية: 0301 basic medicine, Medicine (General), CDK4, Colorectal cancer, Proliferation, MYC, Protein tyrosine phosphatase, QH426-470, medicine.disease_cause, Biochemistry, 03 medical and health sciences, R5-920, PTPN18, 0302 clinical medicine, Full Length Article, Genetics, medicine, Molecular Biology, Genetics (clinical), Chemistry, Protein level, Cell Biology, Cell cycle, medicine.disease, 030104 developmental biology, 030220 oncology & carcinogenesis, Cancer cell, Cancer research, Signal transduction, Carcinogenesis
الوصف: Protein tyrosine phosphatase non-receptor type 18 (PTPN18) is often highly expressed in colorectal cancer (CRC), but its role in this disease remains unclear. We demonstrated that PTPN18 overexpression promotes growth and tumorigenesis in CRC cells and that PTPN18 deficiency yields the opposite results in vitro. Moreover, a xenograft assay showed that PTPN18 deficiency significantly inhibited tumorigenesis in vivo. PTPN18 activated the MYC signaling pathway and enhanced CDK4 expression, which is tightly associated with the cell cycle and proliferation in cancer cells. Finally, we found that MYC interacted with PTPN18 and increased the protein level of MYC. In conclusion, our results suggest that PTPN18 promotes CRC development by stabilizing the MYC protein level, which in turn activates the MYC-CDK4 axis. Thus, PTPN18 could be a novel therapeutic target in the future.
تدمد: 2352-3042
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::78598f0017f5d4f92bbbc81ecfad36a3
https://doi.org/10.1016/j.gendis.2020.08.001
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....78598f0017f5d4f92bbbc81ecfad36a3
قاعدة البيانات: OpenAIRE