ArticleExperimental and therapeutic medicine2020
Ginsenoside Rh2 activates α-catenin phosphorylation to inhibit lung cancer cell proliferation and invasion.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 10 citations in OpenAlex.
- GLI3 in cancer: a context-dependent regulator with diagnostic, prognostic, and therapeutic potential.Frontiers in immunology · 2026Review
- Ginseng-derived compounds as potential anticancer agents targeting cancer stem cells.Journal of ginseng research · 2024Review
- Ginsenoside Rb1 Inhibits the Proliferation of Lung Cancer Cells by Inducing the Mitochondrial-mediated Apoptosis Pathway.Anti-cancer agents in medicinal chemistry · 2024Article
- The ways for ginsenoside Rh2 to fight against cancer: the molecular evidencesJournal of ginseng research · 2023Review
- Ginsenoside Rh2 sensitizes the anti-cancer effects of sunitinib by inducing cell cycle arrest in renal cell carcinoma.Scientific reports · 2022Article
- Ginsenosides emerging as both bifunctional drugs and nanocarriers for enhanced antitumor therapies.Journal of nanobiotechnology · 2021Review
- Expression and prognostic impact of FZDs in pancreatic adenocarcinoma.BMC gastroenterology · 2021Article
- The Crosstalk Between Tumor-Associated Macrophages (TAMs) and Tumor Cells and the Corresponding Targeted Therapy.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The efficacy of ginsenoside Rh2 (Rh2) in cancer therapy has been reported; however, its function in lung cancer remains unknown. To analyze the role of Rh2 in the inhibition of lung cancer cell proliferation in the present study, protein expression levels of E-cadherin, vimentin, β-catenin, Smo, Gli1, and α-catenin were assessed by western blotting, whilst mRNA expression levels of
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.