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Objective: To explore the therapeutic potential of the Dujieqing (DJQ) decoction for multiple myeloma (MM) and elucidate its mechanism of action.
Methods: RPMI8226 cells were treated with DJQ-containing serum (DJQ-CS) and a Wnt/β-catenin pathway inhibitor, XAV-939. Cell counting kit-8 assay was used to examine cell viability, and flow cytometry was performed to examine apoptosis. Real-time polymerase chain reaction and Western blotting were used to evaluate the Wnt/β-catenin pathway family members in the cells. Subsequently, the RPMI8226 cells were subcutaneously injected into the left flank of none obesity disease and server combined immune-deficiency mice to replicate the xenograft tumor mouse models, which were treated with the DJQ decoction for 14 d. Hematoxylin and eosin staining was used to examine the pathological changes of the liver and kidney tissues, and to detect xenograft tumors. Wnt/β-catenin pathway family members were evaluated Western blotting.
Results: DJQ-CS significantly reduced the mRNA and protein expression levels of β-catenin, c-myc, cyclin D1, and lymphoid enhancer binding factor 1 (LEF1) while inhibiting the proliferation of RPMI8226 cells and inducing their apoptosis. Similar results were observed when the Wnt/β-catenin pathway was suppressed by inhibitors. Moreover, in the mouse model of xenograft tumors, DJQ decoction not only reduced the tumor volume but also inhibited the protein levels of β-catenin, c-myc, cyclin D1, and LEF1. The histopathology of the mice also showed increased apoptosis in tumor tissues, while the DJQ decoction treatment did not cause any pathological damage to the kidneys or liver.
Conclusion: Our results indicate that the DJQ decoction suppresses tumor progression by inhibiting the Wnt/β-catenin pathway, offering a promising treatment approach for MM.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340579 | PMC |
http://dx.doi.org/10.19852/j.cnki.jtcm.2025.04.002 | DOI Listing |
Helicobacter pylori (H. pylori), a Gram-negative bacterium, has been classified as a Group I carcinogen by the World Health Organization. It represents the most significant modifiable risk factor for gastric cancer (GC), particularly the intestinal subtype.
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