Oncotarget

Research Papers:

Galectin-1 knockdown improves drug sensitivity of breast cancer by reducing P-glycoprotein expression through inhibiting the Raf-1/AP-1 signaling pathway

Fang Wang, Pengwei Lv, Yuanting Gu, Lin Li _, Xin Ge and Guangcheng Guo

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Oncotarget. 2017; 8:25097-25106. https://doi.org/10.18632/oncotarget.15341

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Abstract

Fang Wang1,*, Pengwei Lv1,*, Yuanting Gu1, Lin Li1, Xin Ge1, Guangcheng Guo1

1Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, 450000, China

*These authors have contributed equally to this work

Correspondence to:

Lin Li, email: [email protected]

Keywords: Galectin-1, multidrug resistance, P-glycoprotein, Raf-1/AP-1, breast cancer

Received: October 19, 2016     Accepted: January 16, 2017     Published: February 15, 2017

ABSTRACT

Galectin-1 (Gal-1), a member of the galectin family of carbohydrate binding proteins, plays a pivotal role in various cellular processes of tumorigenesis. The regulatory effect of Gal-1 on multidrug resistance (MDR) breast cancer cells is still unclear. qRT-PCR and western blot showed that Gal-1 and MDR gene 1 (MDR1) were both highly expressed in breast tumor tissues and cell lines. MTT assay and flow cytometry revealed that Gal-1 knockdown improved sensitivity to paclitaxel (PTX) and adriamycin (ADR) in MCF-7/PTX and MCF-7/ADR cells via inhibition of cell viability and promotion of cell apoptosis, while MDR1 overexpression weakened the sensitivity to PTX and ADR induced by Gal-1 knockdown. Furthermore, the negative effects of Gal-1 knockdown on sensitivity to PTX and ADR in MCF-7/PTX and MCF-7/ADR cells were revealed to be mediated via the suppression of Raf-1/AP-1 pathway. In conclusion, Gal-1 knockdown dramatically improved drug sensitivity of breast cancer by reducing P-glycoprotein (P-gp) expression via inhibiting the Raf-1/AP-1 pathway, providing a novel therapeutic target to overcome MDR in breast cancer.


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