Asset Details
Do you wish to reserve the book?
Bufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor‐κB/MDR1 pathway in colorectal cancer
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Bufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor‐κB/MDR1 pathway in colorectal cancer
Do you wish to request the book?
Bufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor‐κB/MDR1 pathway in colorectal cancer
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Bufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor‐κB/MDR1 pathway in colorectal cancer
2020
Overview
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‐κB signaling mediators and MDR1, while increasing cell chemoresistance. Furthermore, bufalin reverses colorectal cancer MDR by regulating cancer cell stemness through the CD133/nuclear factor‐κB/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. Overexpressing CD133 increases levels of Akt/NF‐κB signaling mediators and MDR1. Bufalin reverses colorectal cancer multidrug resistance by regulating cancer cell stemness via the CD133/NF‐κB/MDR1 pathway.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
