ArticleFrontiers in pharmacology2025
Synergistic anticancer effects of camptothecin and sotorasib in
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
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- Functional and mechanistic inactivation of immune hubs orchestrates tumor development and progression in lung adenocarcinoma.Discover oncology · 2026Article
- Identification and verification of an eight-gene prognostic signature for colorectal cancer based on tumor-associated macrophages.BMC cancer · 2026Article
- E2F1-Driven WDHD1 Transcription Enhances Cell-Cycle Progression and Promotes Pancreatic Cancer Progression.Current oncology (Toronto, Ont.) · 2026Article
- Oxalate induces proliferation and mitochondrial metabolism in select clear cell renal cell carcinoma cell lines.BMC cancer · 2026Article
- Amino acid metabolism-related genes signature correlates with immune infiltration and predicts clinic prognosis in osteosarcoma.BMC cancer · 2026Article
- Reversible Myeloperoxidase Inhibition by Benzodioxole Carboxamides: Insights from In Silico and InVitro Studies.Cell biochemistry and biophysics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sotorasib (AMG510) is a first-in-class irreversible, covalent, and selective KRAS G12C inhibitor. However, in patients, acquired clinical resistance was observed within 1 year of its FDA approval. Researchers are exploring combination and repurposing strategies to help overcome this resistance and improve therapeutic efficacy. Several natural compounds have been extensively investigated for their therapeutic potential against various cancers, both individually and in combination with other chemotherapeutic agents. In this study, we examined the synergistic potential of camptothecin and sotorasib in KRAS G12C-mutated MIA PaCa-2 and KRAS G12D-mutated PANC-1 pancreatic ductal adenocarcinoma (PDAC) cells. Methods: We assessed the half maximal inhibitory concentration (IC50) values of camptothecin and sotorasib using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and predicted their synergistic potential using combination index (CI) values and isobologram plots. Proliferation, wound healing, and colony formation assays were performed to examine the chemotherapeutic potential of camptothecin and sotorasib (combination and monotherapy). Reactive oxygen species induction, DNA fragmentation, autophagy flux, and apoptosis and cell cycle analyses were performed using 2',7'-dichlorofluorescein diacetate (DCFH-DA), 4',6-diamidino-2-phenylindole (DAPI), LC3-II quantification assays, and flow cytometry analysis. Furthermore, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to analyze gene expression patterns in both pancreatic ductal adenocarcinoma cell lines. Additionally, network pharmacology, gene ontology, and Kyoto Encyclopedia of and Genomes pathway enrichment were performed for camptothecin in PDAC. Results: The combination therapy with camptothecin and sotorasib resulted in significantly inhibited proliferation, migration, and colony formation; elevated intracellular ROS levels; and induced DNA fragmentation compared with monotherapies in both PDAC cell lines. Flow cytometry and cell cycle analysis revealed that the combination treatment induced apoptosis and G1/S cell cycle arrest. Furthermore, qRT-PCR analysis revealed that the combination therapy significantly upregulated pro-apoptotic genes and downregulated KRAS pathway-related genes, cleaved poly (ADP-ribose) polymerase, anti-apoptotic-related genes as well as autophagy-related genes in both PDAC cell lines. Network pharmacology analysis supports that the identified hub genes play a role in apoptosis and autophagy. Conclusion: We observed a synergistic relationship between camptothecin and sotorasib in
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