ArticleCancer biomarkers : section A of Disease markers2025
Panax notoginseng improves the sensitivity of non-small cell lung cancer to cisplatin by inhibiting Akt signaling.
Article in Cancer biomarkers : section A of Disease markers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Sulforaphane attenuates cisplatin‑induced acute kidney injury by inhibiting oxidative stress, inflammation and apoptosis via regulation of NRF2.Molecular medicine reports · 2026Article
- TRIM46 deficiency‑induced DNA damage enhances the sensitivity of cisplatin in non‑small cell lung cancer by regulating the Akt signaling pathway.Oncology reports · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BackgroundCisplatin (DDP) resistance is a major challenge in the management of non-small cell lung cancer (NSCLC). Panax notoginseng has anticancer effects on a variety of solid tumors, but data on NSCLC and DDP resistance are lacking.ObjectiveTo investigate the effect of Panax notoginseng on DDP resistance in NSCLC in vitro and in vivo and explore the mechanisms involved.MethodsA 1 g/mL Panax notoginseng extract was prepared to treat the A549 and DDP-resistant A549/DDP cell lines. Cell proliferation was assessed using the CCK-8 assay, and apoptosis was measured via Annexin V-FITC/PI staining and flow cytometry. Glucose uptake, ATP production, and lactate levels were evaluated. Protein levels of p-AKT, GLUT1, HKII, and cleaved-caspase-3 were analyzed by Western blot. IGF1 was used to activate the Akt pathway. In vivo, A549/DDP cells were inoculated into nude mice to establish subcutaneous tumors, and tumor growth and apoptosis were assessed.ResultsPanax notoginseng inhibited A549/DDP cell proliferation, enhanced DDP-induced apoptosis, and reduced glucose uptake, ATP, and lactate levels (all
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