ArticleCell division2024
Anti-cancer effects of Coix seed extract through KCTD9-mediated ubiquitination of TOP2A in lung adenocarcinoma.
Article in Cell division, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- 8 specific Chinese herbal injections combined with chemotherapy for breast cancer: a systematic review and network meta-analysis of comparative safety and efficacy.Frontiers in pharmacology · 2025Pooled it
- Global trends and projections of tracheal, bronchial, and lung cancer (TBL) associated with secondhand smoke (SHS) exposure in women: insights of the Global Burden of Disease (GBD) study 2021 from 1990 to 2021 and prediction to 2035.Journal of thoracic disease · 2026Article
- Genome-wide analysis of DGAT gene family in Coix lacryma jobi L. and functional characterization in yeast H1246.BMC plant biology · 2025Article
- Enhancement of apoptosis in HCT116 and HepG2 cells byChinese herbal medicines · 2025Article
- Analysis of the correlation between the distribution of microorganisms carried byCurrent research in food science · 2025Article
- HJURP modulates cell proliferation and chemoresistance via the MYC/TOP2A transcriptional axis in gastric cancer.Frontiers in molecular biosciences · 2025Article
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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
backgroundCoix seed extract (CSE), a traditional Chinese medicine, has been reported as an adjunctive therapy in cancers. However, the molecular targets are largely unclear. The study is designed to unveil its function in lung adenocarcinoma (LUAD) and the possible molecular mechanism.
methodsThe HERB database was utilized to predict the molecular targets of the Coix seed, followed by prognostic value prediction in the Kaplan-Meier Plotter database. LUAD cells were infected with sh-KCTD9 after co-culture with CSE, and cell viability, growth, proliferation, and apoptosis were determined. The substrates of KCTD9 were predicted using a protein-protein interaction network and verified. The expression of PD-L1, the contents of TNF-α, IFN-γ, CXCL10, and CXCL9 in the co-culture system of LUAD cells and T cells and the proliferation of T cells were evaluated to study the immune escape of LUAD cells in response to CSE and sh-KCTD9. Lastly, tumor growth and immune escape were observed in tumor-bearing mice.
resultsCSE inhibited malignant behavior and immune escape of LUAD cells, and the reduction of KCTD9 reversed the inhibitory effect of CSE on malignant behavior and immune escape of LUAD cells. Knockdown of KCTD9 expression inhibited ubiquitination modification of TOP2A, and knockdown of TOP2A suppressed immune escape of LUAD cells in the presence of knockdown of KCTD9. CSE exerted anticancer effects in mice, but the reduction of KCTD9 partially compromised the anticancer effect of CSE.
conclusionCSE inhibits immune escape and malignant progression of LUAD through KCTD9-mediated ubiquitination modification of TOP2A.
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