Prostaglandin F
Colorectal cancer
DNA damage
Drug resistance
Oxaliplatin
Prostaglandin F2αsynthase
Journal
World journal of gastroenterology
ISSN: 2219-2840
Titre abrégé: World J Gastroenterol
Pays: United States
ID NLM: 100883448
Informations de publication
Date de publication:
21 Oct 2023
21 Oct 2023
Historique:
received:
03
07
2023
revised:
14
09
2023
accepted:
26
09
2023
medline:
31
10
2023
pubmed:
30
10
2023
entrez:
30
10
2023
Statut:
ppublish
Résumé
Oxaliplatin (Oxa) is the first-line chemotherapy drug for colorectal cancer (CRC), and Oxa resistance is crucial for treatment failure. Prostaglandin F To explore the role and related mechanisms of PGFS in mediating Oxa resistance in CRC. The PGFS expression level was examined in 37 pairs of CRC tissues and paracancerous tissues at both the mRNA and protein levels. Overexpression or knockdown of PGFS was performed in CRC cell lines with acquired Oxa resistance (HCT116-OxR and HCT8-OxR) and their parental cell lines (HCT116 and HCT8) to assess its influence on cell proliferation, chemoresistance, apoptosis, and DNA damage. For determination of the underlying mechanisms, CRC cells were examined for platinum-DNA adducts and reactive oxygen species (ROS) levels in the presence of a PGFS inhibitor or its products. Both the protein and mRNA levels of PGFS were increased in the 37 examined CRC tissues compared to the adjacent normal tissues. Oxa induced PGFS expression in the parental HCT116 and HCT8 cells in a dose-dependent manner. Furthermore, overexpression of PGFS in parental CRC cells significantly attenuated Oxa-induced proliferative suppression, apoptosis, and DNA damage. In contrast, knockdown of PGFS in Oxa-resistant HCT116 and HCT8 cells (HCT116-OxR and HCT8-OxR) accentuated the effect of Oxa treatment PGFS promotes resistance to Oxa in CRC
Sections du résumé
BACKGROUND
BACKGROUND
Oxaliplatin (Oxa) is the first-line chemotherapy drug for colorectal cancer (CRC), and Oxa resistance is crucial for treatment failure. Prostaglandin F
AIM
OBJECTIVE
To explore the role and related mechanisms of PGFS in mediating Oxa resistance in CRC.
METHODS
METHODS
The PGFS expression level was examined in 37 pairs of CRC tissues and paracancerous tissues at both the mRNA and protein levels. Overexpression or knockdown of PGFS was performed in CRC cell lines with acquired Oxa resistance (HCT116-OxR and HCT8-OxR) and their parental cell lines (HCT116 and HCT8) to assess its influence on cell proliferation, chemoresistance, apoptosis, and DNA damage. For determination of the underlying mechanisms, CRC cells were examined for platinum-DNA adducts and reactive oxygen species (ROS) levels in the presence of a PGFS inhibitor or its products.
RESULTS
RESULTS
Both the protein and mRNA levels of PGFS were increased in the 37 examined CRC tissues compared to the adjacent normal tissues. Oxa induced PGFS expression in the parental HCT116 and HCT8 cells in a dose-dependent manner. Furthermore, overexpression of PGFS in parental CRC cells significantly attenuated Oxa-induced proliferative suppression, apoptosis, and DNA damage. In contrast, knockdown of PGFS in Oxa-resistant HCT116 and HCT8 cells (HCT116-OxR and HCT8-OxR) accentuated the effect of Oxa treatment
CONCLUSION
CONCLUSIONS
PGFS promotes resistance to Oxa in CRC
Identifiants
pubmed: 37900995
doi: 10.3748/wjg.v29.i39.5452
pmc: PMC10600807
doi:
Substances chimiques
Oxaliplatin
04ZR38536J
Platinum
49DFR088MY
DNA Adducts
0
Reactive Oxygen Species
0
RNA, Messenger
0
Prostaglandins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5452-5470Informations de copyright
©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflict-of-interest statement: The authors declare that there are no conflicts of interest in our study.
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