Abstract 4734: Inhibitory effects of metformin on epithelial-mesenchymal transition of CD44+/CD117+ ovarian cancer stem cells

Author(s):  
Gary G. Xiao ◽  
Rongrong Zhang ◽  
Ping Zhang ◽  
Hong Wang ◽  
Dongming Hou ◽  
...  
2019 ◽  
Author(s):  
Monica Angelica Amaya Padilla ◽  
Mudra Binju ◽  
Graeme Wan ◽  
Yohan Suryo Rahmanto ◽  
Pritinder Kaur ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4178
Author(s):  
Andrzej Nowicki ◽  
Magdalena Kulus ◽  
Maria Wieczorkiewicz ◽  
Wojciech Pieńkowski ◽  
Katarzyna Stefańska ◽  
...  

Despite the increasing development of medicine, ovarian cancer is still a high-risk, metastatic disease that is often diagnosed at a late stage. In addition, difficulties in its treatment are associated with high resistance to chemotherapy and frequent relapse. Cancer stem cells (CSCs), recently attracting significant scientific interest, are considered to be responsible for the malignant features of tumors. CSCs, as the driving force behind tumor development, generate new cells by modifying different signaling pathways. Moreover, investigations on different types of tumors have shown that signaling pathways are key to epithelial-mesenchymal transition (EMT) regulation, metastasis, and self-renewal of CSCs. Based on these established issues, new therapies are being investigated based on the use of inhibitors to block CSC growth and proliferation signals. Many reports indicate that CSC markers play a key role in cancer metastasis, with hopes placed in their targeting to block this process and eliminate relapses. Current histological classification of ovarian tumors, their epidemiology, and the most recent knowledge of ovarian CSCs, with particular emphasis on their molecular background, are important aspects for consideration. Furthermore, the importance of signaling pathways involved in tumor growth, development, and metastasis, is also presented.


Oncotarget ◽  
2016 ◽  
Vol 7 (34) ◽  
pp. 55771-55788 ◽  
Author(s):  
Junli Deng ◽  
Li Wang ◽  
Hongmin Chen ◽  
Jingli Hao ◽  
Jie Ni ◽  
...  

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