ArticleScientific reports2016
Platycodin D potentiates proliferation inhibition and apoptosis induction upon AKT inhibition via feedback blockade in non-small cell lung cancer cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest.Oncology reports · 2026Article
- Genomic Analysis and Clinical Correlation of Non-Small Cell Lung Cancer with Special Reference to Brain Metastasis.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Research progress on the bioactivity of platycodin D from Platycodon grandifloras.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Platycodon grandiflorum-derived extracellular vesicles suppress triple-negative breast cancer growth by reversing the immunosuppressive tumor microenvironment and modulating the gut microbiota.Journal of nanobiotechnology · 2025Article
- [Platycodin D improves pulmonary fibrosis in mice by down-regulating TRPC6 expression and reducing ROS production in lung fibroblasts].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- From immune checkpoints to therapies: understanding immune checkpoint regulation and the influence of natural products and traditional medicine on immune checkpoint and immunotherapy in lung cancer.Frontiers in immunology · 2024Review
- Tumor-targeted liposomes with platycodin D2 promote apoptosis in colorectal cancer.Materials today. Bio · 2023Review
- Chromosome-Scale Genome Assembly and Triterpenoid Saponin Biosynthesis in Korean Bellflower (International journal of molecular sciences · 2023Article
- Biotransformation of Platycosides, Saponins from Balloon Flower Root, into Bioactive Deglycosylated Platycosides.Antioxidants (Basel, Switzerland) · 2023Review
- The pharmacology and mechanisms of platycodin D, an active triterpenoid saponin fromFrontiers in pharmacology · 2023Review
- Article
- The disruption of protein-protein interactions with co-chaperones and client substrates as a strategy towards Hsp90 inhibition.Acta pharmaceutica Sinica. B · 2021Review
- Combined Anti-Cancer Effects of Platycodin D and Sorafenib on Androgen-Independent and PTEN-Deficient Prostate Cancer.Frontiers in oncology · 2021Article
- Suppressive effect of platycodin D on bladder cancer through microRNA-129-5p-mediated PABPC1/PI3K/AKT axis inactivation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- Effects of Platycodin D on apoptosis, migration, invasion and cell cycle arrest of gallbladder cancer cells.Oncology letters · 2020Article
- A Systems-Level Analysis of Mechanisms ofMolecules (Basel, Switzerland) · 2018Review
- Anti-Inflammatory Activities of Compounds Isolated from the Rhizome ofMolecules (Basel, Switzerland) · 2018Article
- Targeting the Hsp90-Cdc37-client protein interaction to disrupt Hsp90 chaperone machinery.Journal of hematology & oncology · 2018Review
- Anticancer drug discovery from Chinese medicinal herbs.Chinese medicine · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKT is the frequently overexpressed and constitutively active kinase within NSCLC cells and recognized as a promising target for NSCLC treatment. However, AKT inhibition relieves the feedback inhibition of upstream receptor tyrosine kinases (RTKs) that may weaken the efficiency of AKT inhibitors. Platycodin D (PD), isolated from widely-used traditional Chinese medicine Platycodonis Radix, is now found to remarkably enhance the anti-proliferative effect of AKT inhibitors. In this study, combinatorial activity of AKT inhibitor MK2206 and PD on cell proliferation, apoptosis and related signaling were disclosed. Long-term AKT inhibition induced up-regulation of RTKs, including EGFR and HER-2. Co-treatment of MK2206 with PD could abolish this feedback survival through decrease of EGFR, HER-2, and p-AKT, and profound inhibition of 4E-BP1, leading to an amplified anti-proliferative and apoptotic activity in NSCLC cells. Similarly, feedback activation in response to reduction of AKT expression by small interfering RNA (siRNA) was also blocked by PD and apoptotic effect was further enhanced. Thus, PD potentiated proliferative inhibition and apoptotic induction of both AKT inhibitor and siRNA. These findings also reveal the limitations of suppressing feedback-regulated pathways by monotherapy and establish a mechanistic rationale for a novel combination approach targeting AKT for the treatment of NSCLC.
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