Interference of Frizzled 1 (FZD1) reverses multidrug resistance in breast cancer cells through the Wnt/β-catenin pathway
H Zhang, X Zhang, X Wu, W Li, P Su, H Cheng, L Xiang… - Cancer letters, 2012 - Elsevier
H Zhang, X Zhang, X Wu, W Li, P Su, H Cheng, L Xiang, P Gao, G Zhou
Cancer letters, 2012•ElsevierMultidrug resistance (MDR) represents a major obstacle in the successful treatment of breast
cancer. The MDR1 gene is a direct target of the Wnt/β-catenin signaling pathway, which
controls tumor development. Overexpression of P-glycoprotein, encoded by the MDR1 gene,
is one of the most common causes of MDR. We found that the Frizzled 1 (FZD1) protein,
which is an essential component of the Wnt/β-catenin pathway, is overexpressed in the
multidrug resistant breast cancer cell subline MCF-7/ADM, coincident with MDR1/P-gp …
cancer. The MDR1 gene is a direct target of the Wnt/β-catenin signaling pathway, which
controls tumor development. Overexpression of P-glycoprotein, encoded by the MDR1 gene,
is one of the most common causes of MDR. We found that the Frizzled 1 (FZD1) protein,
which is an essential component of the Wnt/β-catenin pathway, is overexpressed in the
multidrug resistant breast cancer cell subline MCF-7/ADM, coincident with MDR1/P-gp …
Multidrug resistance (MDR) represents a major obstacle in the successful treatment of breast cancer. The MDR1 gene is a direct target of the Wnt/β-catenin signaling pathway, which controls tumor development. Overexpression of P-glycoprotein, encoded by the MDR1 gene, is one of the most common causes of MDR. We found that the Frizzled 1 (FZD1) protein, which is an essential component of the Wnt/β-catenin pathway, is overexpressed in the multidrug resistant breast cancer cell subline MCF-7/ADM, coincident with MDR1/P-gp. FZD1 silencing induced down-regulation of MDR1/P-gp, restored sensitivity to four chemotherapy drugs, and significantly decreased cytoplasmic and nuclear β-catenin levels. FZD1 appears to mediate multidrug resistance by regulating the Wnt/β-catenin pathway.
Elsevier