Title of article :
PKM2 Promotes Breast Cancer Progression by Regulating Epithelial Mesenchymal Transition
Author/Authors :
Xiao, Hui The Second Hospital - Cheeloo College of Medicine - Shandong University, Jinan, Shandong, China , Zhang, Longxiao The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China , Chen, Yuan The Second Hospital - Cheeloo College of Medicine - Shandong University, Jinan, Shandong, China , Zhou, Chengjun The Second Hospital - Cheeloo College of Medicine - Shandong University, Jinan, Shandong, China , Wang, Xiao The Second Hospital - Cheeloo College of Medicine - Shandong University, Jinan, Shandong, China , Wang, Dehai The Second Hospital - Cheeloo College of Medicine - Shandong University, Jinan, Shandong, China , Liu, Zhenzhong The Second Hospital - Cheeloo College of Medicine - Shandong University, Jinan, Shandong, China
Pages :
9
From page :
1
To page :
9
Abstract :
Breast cancer is the leading cause of females characterized by high invasive potential. It is necessary to explore the underlying mechanism of breast cancer metastases and to find specific therapeutic targets. PKM2 is considered a new biomarker of cancer with upregulated expression in tumor tissue. PKM2 participates in the cancer-specific Warburg effect to regulate fast glucose intake consumption. Besides, PKM2 also contributes to cancer progression, especially tumor metastasis. In this study, we showed that PKM2 is upregulated in breast cancer tissues and the upregulating of PKM2 in breast cancer correlates with poor prognosis. PKM2 can regulate tumor progression by promoting tumor cell viability and mobility. Furthermore, overexpression of PKM2 can promote EMT to encourage tumor metastasis. These findings indicate PKM2 is a potentially useful diagnostic biomarker and therapeutic target in breast cancer.
Farsi abstract :
فاقد چكيده فارسي
Keywords :
Breast Cancer , Regulating Epithelial Mesenchymal Transition , PKM2 Promotes
Journal title :
Analytical Cellular Pathology
Serial Year :
2020
Full Text URL :
Record number :
2605590
Link To Document :
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