ReferenceID 1374
Bufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor-κB/MDR1 pathway in colorectal cancer
Cancer Sci
Recent studies have shown that MDR could be induced by the high stemness of cancer cells. In a previous study, we found bufalin could reverse MDR and inhibit cancer cell stemness in colorectal cancer, but the relationshi
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Record Fields
Scalar fields from the final reference record.
- Reference Id
- 1374
- Evidence Id
- 17964
- Core Evidence Id
- 17964
- Source Reference Id
- 2763
- Herb2 Reference Id
- HBREF003560
- Subject Paper Key
- HBIN018981_32058643
- Pubmed Id
- 32058643
- Doi
- 10.1111/cas.14345
- Paper Title
- Bufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor-κB/MDR1 pathway in colorectal cancer
- Paper Abstract
- Recent studies have shown that MDR could be induced by the high stemness of cancer cells. In a previous study, we found bufalin could reverse MDR and inhibit cancer cell stemness in colorectal cancer, but the relationship between them was unclear. Here we identified overexpressing CD133 increases levels of Akt/nuclear factor-kappaB signaling mediators and MDR1, while increasing cell chemoresistance. Furthermore, bufalin reverses colorectal cancer MDR by regulating cancer cell stemness through the CD133/nuclear factor-kappaB/MDR1 pathway in vitro and in vivo. Taken together, our results suggest that bufalin could be developed as a novel 2-pronged drug that targets CD133 and MDR1 to eradicate MDR cells and could ultimately be combined with conventional chemotherapeutic agents to improve treatment outcomes for patients with colorectal cancer.
- Journal
- Cancer Sci
- Publish Year
- 2020
- Experiment Subject
- patient; mdr cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Cancer; Colorectal Cancer
- Paper Title Cn
- Paper Title En
- Bufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor-κB/MDR1 pathway in colorectal cancer
- Bilingual Status
- semi_complete