Cargando…
Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer
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 pathw...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632425/ https://www.ncbi.nlm.nih.gov/pubmed/34858519 http://dx.doi.org/10.1155/2021/6350038 |
_version_ | 1784607752118599680 |
---|---|
author | Zhu, Yingping Xu, Leilai Ma, Weirong Chen, Zeliang |
author_facet | Zhu, Yingping Xu, Leilai Ma, Weirong Chen, Zeliang |
author_sort | Zhu, Yingping |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8632425 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-86324252021-12-01 Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer Zhu, Yingping Xu, Leilai Ma, Weirong Chen, Zeliang Comput Math Methods Med Research Article 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. Hindawi 2021-11-23 /pmc/articles/PMC8632425/ /pubmed/34858519 http://dx.doi.org/10.1155/2021/6350038 Text en Copyright © 2021 Yingping Zhu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhu, Yingping Xu, Leilai Ma, Weirong Chen, Zeliang Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer |
title | Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer |
title_full | Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer |
title_fullStr | Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer |
title_full_unstemmed | Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer |
title_short | Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer |
title_sort | research on radiosensitivity of the protein kinase b signaling pathway in cervical cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632425/ https://www.ncbi.nlm.nih.gov/pubmed/34858519 http://dx.doi.org/10.1155/2021/6350038 |
work_keys_str_mv | AT zhuyingping researchonradiosensitivityoftheproteinkinasebsignalingpathwayincervicalcancer AT xuleilai researchonradiosensitivityoftheproteinkinasebsignalingpathwayincervicalcancer AT maweirong researchonradiosensitivityoftheproteinkinasebsignalingpathwayincervicalcancer AT chenzeliang researchonradiosensitivityoftheproteinkinasebsignalingpathwayincervicalcancer |