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conferenceseries
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Volume 10
Journal of Cancer Science & Therapy
Oncologists 2018
May 24-25, 2018
May 24-25, 2018 Osaka, Japan
22
nd
Global Annual Oncologists Meeting
Abrogation of glutathione peroxidase-1 drives EMT and chemoresistance in pancreatic cancer by
activating ROS-mediated Akt/GSK3β/snail signaling
Qingcai Meng, Si Shi, Chen Liang, Jie Hua, Yiyin Zhang, Jin Xu and Xianjun Yu
Fudan University, China
Introduction & Purpose:
Pancreatic Ductal Adenocarcinoma (PDAC) remains one of the deadliest cancers worldwide, partly
due to tumor chemoresistance. Numerous studies have shown that Glutathione Peroxidase-1 (GPx1) plays various roles in
development and progression of multiple tumors. However, its role in pancreatic cancer remains unclear. In this study, we
sought to elucidate the function of GPx1 in pancreatic cancer malignancy and gemcitabine (GEM) resistance.
Experimental Design:
PDAC tissue microarrays were used to evaluate the correlation between GPx1 expression and
clinicopathological features. Cytobiology, molecular biology assays and mouse models were performed to investigate the
detailed mechanisms. Finally, RNA-sequencing was performed in the scramble-shRNA and GPx1-shRNA MiaPaCa-2 cells to
identify core signaling pathways.
Result:
The level of GPx1 expression was negatively associated with Overall Survival (OS) in patients with PDAC. Silencing of
GPx1 resulted in an Epithelial-Mesenchymal Transition (EMT) phenotype and increased chemoresistance to GEM in vitro and
in vivo. Additionally, activation of Akt/GSK3β/snail signaling was demonstrated to be involved in this process.
Conclusion:
Our results reveal that GPx1 could inhibit EMT and chemoresistance by regulating Akt/GSK3β/Snail axis in
PDAC.
15216633283@163.comJ Cancer Sci Ther 2018, Volume 10
DOI: 10.4172/1948-5956-C3-130