Cisplatin induces chemoresistance through the PTGS2-mediated anti-apoptosis in gastric cancer
Abstract
It has been proposed that the aberrant expressions of the classical apoptosis-related genes and the subsequent decrease of apoptosis contribute to the development of cisplatin resistance in gastric cancer. However, little is known about the correlation and the molecular regulation mechanisms of cisplatin and the apoptosis-related gene expressions. Herein, we first identified the expressions of the anti-apoptotic BCL2 and the prostaglandin-endoperoxide synthase-2 (PTGS2) genes, which were abundant in the gastric carcinoma and associated with poor patient survival, were closely related with the resistance against cisplatin. Further investigations revealed that PTGS2 served as an essential mediator involved in the developing process of the resistance against cisplatin via mediating the inhibition effects of cisplatin on BCL2 expression. Mechanistically, cisplatin induced PTGS2 expression through ROS/NF-κB pathway. In addition, PTGS2 mediated cisplatin-induced BCL2 expression and subsequent resistance to apoptosis via PGE2/EP4/MAPKs (ERK1/2, P38) axis. Analysis of the clinical specimens demonstrated that PTGS2 and BCL2 were positively correlated in human gastric cancer. Moreover, in the xenograft models, inhibition of PTGS2 by celecoxib significantly augmented the cytotoxic efficacy of cisplatin in the resistant gastric cancer via suppression of PTGS2 and BCL2 expressions regulated by ERK1/2 and P38 signal axis, suggesting PTGS2 might be employed as an adjunctive therapeutic target for reversal of the chemoresistance in a subset of cisplatin resistant gastric cancer.
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PTGS2 reduces the cytotoxic effects of cisplatin on gastric cancer cells through the PGE2/EP4/MAPKs axis.
“PTGS2 has also been shown to reduce the cytotoxic effects of cisplatin (DDP) on GC cells through the PGE2/EP4/MAPKs (ERK1/2 and P38) axis.179”
From Drug repurposing for cancer therapy (2024) · cites this paper as [179]
Celecoxib enhances the chemosensitivity of platinum-treated gastric cancer cells through inhibition of PTGS2 and Bcl2 expression via the ERK1/2 and P38 signaling axis.
“Celecoxib has been shown to enhance the chemosensitivity of platinum-treated GC cells through the inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) and Bcl2 expression via the ERK1/2 and P38 signaling axis.”
From Drug repurposing for cancer therapy (2024) · cites this paper as [179]
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- Authors
- Lin, X.-M., Li, S., Zhou, C., Li, R.-Z., Wang, H., Luo, W., Huang, Y.-S., Chen, L.-K., Cai, J.-L., Wang, T.-X., Zhang, Q.-H., Cao, H., & Wu, X.-P.
- Affiliations
- Jinan University (CN)
- Jiangxi Provincial People's Hospital (CN)
- Corresponding author
- Cao, Hong
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2019-11
- Volume
- 116
- Pages
- 105610
- ISSN
- 1357-2725 (ISSN-L)
- OpenAlex
- W2973038909
- Cited by
- 43
- References
- 47
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 7 · 2023: 7 · 2022: 8 · 2021: 8 · 2020: 3
- FWCI
- 2.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Opening Project of Zhejiang Provincial Top Key Discipline of Pharmaceutical Sciences
- National Natural Science Foundation of China (81573334)
- Science and Technology Planning Project of Guangdong Province (2015A020211017, 2017A020211029)
- Topics
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Gastric Cancer Management and Outcomes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- cisplatin resistance, gastric cancer, cyclooxygenase-2, Bcl-2, apoptosis, prostaglandin E2, EP4 receptor, MAPK signaling, ERK1/2, p38 MAPK, NF-κB, reactive oxygen species, celecoxib, chemoresistance reversal
- MeSH terms
- Celecoxib, Animals, Antineoplastic Agents, Cisplatin, Humans, Male, Mice, Nude, Stomach Neoplasms, Dinoprostone, Signal Transduction, Gene Expression Regulation, Neoplastic, Survival Analysis, NF-kappa B, Reactive Oxygen Species, Drug Resistance, Neoplasm, Proto-Oncogene Proteins c-bcl-2, Mitogen-Activated Protein Kinase 1, Xenograft Model Antitumor Assays, Cell Line, Tumor, Tumor Burden, p38 Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 3, Mice, Cyclooxygenase 2, Receptors, Prostaglandin E, EP4 Subtype
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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