ArticleFrontiers in oncology2022
Gou Qi Zi inhibits proliferation and induces apoptosis through the PI3K/AKT1 signaling pathway in non-small cell lung cancer.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Multi-omics investigation of per- and polyfluoroalkyl substances in lung adenocarcinoma: comprehensive network toxicology, machine learning and molecular docking experiments.Molecular diversity · 2026Article
- Kang Ru Plus reverses osimertinib resistance in lung adenocarcinoma via suppression of EGFR/PI3K/AKT signaling.American journal of cancer research · 2026Article
- [Inhibitory effect ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Extended survival of a patient with gastrointestinal multiple malignancies managed with anti-PD-1 immunotherapy: a case report.Immunotherapy · 2025Article
- Network pharmacology and UHPLC-HRMS reveal the mechanism of QSFZYL and BMSCs overexpressing IFN-γ against lung adenocarcinoma.Frontiers in immunology · 2025Article
- Advances in research on the effects of medicinal and edible substances on lung cancer: an updated review.Frontiers in pharmacology · 2025Review
- Article
- Long‑term survival of a patient with advanced lung cancer treated with targeted therapy and anti‑PD‑1 immunotherapy as multi‑line therapy: A case report.Oncology letters · 2024Article
- Jatrophone: a cytotoxic macrocylic diterpene targeting PI3K/AKT/NF-κB pathway, inducing apoptosis and autophagy in resistant breast cancer cells.BMC complementary medicine and therapies · 2023Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Gou Qi Zi ( Methods: The TCMSP, TCMID, SwissTargetPrediction, DrugBank, DisGeNET, GeneCards, OMIM and TTD databases were searched for the active components of Gou Qi Zi and their potential therapeutic targets in NSCLC. Protein-protein interaction networks were identified and the interactions of target proteins were analyzed. Involved pathways were determined by GO enrichment and KEGG pathway analyses using the Metascape database, and molecular docking technology was used to study the interactions between active compounds and potential targets. These results were verified by cell counting kit-8 assays, BrdU labeling, flow cytometry, immunohistochemistry, western blotting, and qRT-PCR. Results: Database searches identified 33 active components in Gou Qi Zi, 199 predicted biological targets and 113 NSCLC-related targets. A network of targets of traditional Chinese medicine compounds and potential targets of Gou Qi Zi in NSCLC was constructed. GO enrichment analysis showed that Gou Qi Zi targeting of NSCLC was mainly due to the effect of its associated lipopolysaccharide. KEGG pathway analysis showed that Gou Qi Zi acted mainly through the PI3K/AKT1 signaling pathway in the treatment of NSCLC. Molecular docking experiments showed that the bioactive compounds of Gou Qi Zi could bind to AKT1, C-MYC and TP53. These results were verified by experimental assays. Conclusion: Gou Qi Zi induces apoptosis and inhibits proliferation of NSCLC
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