c-Myc promotes tumor proliferation and anti-apoptosis by repressing p21 in rhabdomyosarcomas
| Autor: | Jinsong Li, Na Song, Weixing Zhao, Haijun Wang, Dan Zang, Wenyu Di, Jinghang Zhang, Jian Yu, Ruina Guo |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine Cancer Research Transcription Genetic genetic structures Carcinogenesis Cell Apoptosis medicine.disease_cause Biochemistry 0302 clinical medicine Rhabdomyosarcoma Child biology Cell Cycle Middle Aged Cell cycle Gene Expression Regulation Neoplastic medicine.anatomical_structure Oncology Child Preschool 030220 oncology & carcinogenesis Molecular Medicine Female Cyclin-Dependent Kinase Inhibitor p21 musculoskeletal diseases Adolescent Proto-Oncogene Proteins c-myc Young Adult 03 medical and health sciences Cyclin-dependent kinase Cell Line Tumor Genetics medicine Humans RNA Messenger Molecular Biology Aged Cell Proliferation Oncogene medicine.disease Molecular medicine Thiazoles 030104 developmental biology biology.protein Cancer research human activities |
| Zdroj: | Molecular Medicine Reports. 16:4089-4094 |
| ISSN: | 1791-3004 1791-2997 |
| Popis: | v-myc avian myelocytomatosis viral oncogene homolog (c-Myc) is an important member protein of the Myc family that is important in cell cycle progression, apoptosis and tumorigenesis. In the present study, the role of c‑Myc in rhabdomyosarcoma (RMS) was assessed. Firstly, expression of endogenous c‑Myc and cyclin dependent kinase inhibitor 1A (p21) was examined in normal skeletal muscle, RMS specimens and TE671 RMS cells by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. Furthermore, cell cycle progression and apoptosis were assessed in TE671 RMS cells following treatment with a c‑Myc inhibitor, 10058‑F4. The results demonstrated that c‑Myc was overexpressed in clinical RMS tissues and TE671 cells, with the highest expression observed in the most RMS samples. Expression of p21 protein and apoptosis function were increased following treatment with 10058‑F4, but no difference was observed in cell cycle progression. In conclusion, the present study indicated that c‑Myc promotes RMS development by inhibiting apoptosis through repression of p21 transcription. Further studies will be required to evaluate c‑Myc as a target for RMS clinical treatment. |
| Databáze: | OpenAIRE |
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