Open AccessBufalin reverses multidrug resistance by regulating stemness through the CD133/nuclear factor‐κB/MDR1 pathway in colorectal cancer
Author(s) -
Zhan Yueping,
Qiu Yanyan,
Wang Haijing,
Wang Ziyuan,
Xu Jian,
Fan Guohua,
Xu Jianhua,
Li Wei,
Cao Yijun,
Le VanMinh,
Ly HaiTrieu,
Yuan Zeting,
Xu Ke,
Yin Peihao
Publication year - 2020
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.14345
Subject(s) - bufalin , cancer , colorectal cancer , cancer research , cancer stem cell , multiple drug resistance , cancer cell , medicine , biology , pharmacology , drug resistance , apoptosis , biochemistry , genetics
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.