Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer
| Autor: | Yingping Zhu, Weirong Ma, Leilai Xu, Zeliang Chen |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
MAPK/ERK pathway
Article Subject MAP Kinase Signaling System Computer applications to medicine. Medical informatics R858-859.7 Uterine Cervical Neoplasms Radiation Tolerance General Biochemistry Genetics and Molecular Biology HeLa Cell Line Tumor Humans Radiosensitivity Telomerase Protein kinase B General Immunology and Microbiology biology Cell growth Applied Mathematics Computational Biology General Medicine biology.organism_classification Gene Expression Regulation Neoplastic Apoptosis Gene Knockdown Techniques Modeling and Simulation Protein kinase B signaling Cancer research Female Signal transduction Proto-Oncogene Proteins c-akt HeLa Cells Signal Transduction Transcription Factors Research Article |
| Zdroj: | Computational and Mathematical Methods in Medicine, Vol 2021 (2021) Computational and Mathematical Methods in Medicine |
| ISSN: | 1748-6718 1748-670X |
| DOI: | 10.1155/2021/6350038 |
| Popis: | The main characteristics of cervical cancer are abnormal and uncontrolled cell proliferation, and it regulates cell growth, differentiation, and cell death through genetic and epigenetic changes. This paper mainly discusses the radiosensitivity of the cervical cancer protein kinase B signaling pathway and discusses the specific mechanisms that affect the occurrence and development of cervical cancer. In addition, this paper studies the effect of transient transfection knocking down the expression of TRIP4 in cervical cancer cells on the expression of key proteins in related signaling pathways and explores the mechanism of its specific effects and finds the mechanism of TRIP4’s effect on cervical cancer radiosensitivity. The findings of this study show for the first time that knocking down TRIP4 inhibits cell viability by inhibiting the P13K/AKT and MAPK/ERK pathways, and this corresponds to the first part of the experimental results, which show that knocking down TRIP4 inhibits colony formation and increases apoptosis in HeLa and SiHa cells. Moreover, simultaneous inhibition of TRIP4 and hTERT proteins can increase the radiosensitivity of cervical cancer cells. These findings indicate that the inhibition of TRIP4 may be a new type of treatment that selectively targets the P13K/AKT and MAPK/ERK pathways and hTERT pathways in cervical cancer cells and provides a therapeutic option for the treatment of cervical cancer. |
| Databáze: | OpenAIRE |
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