scholarly journals Luteinizing hormone facilitates angiogenesis in ovarian epithelial tumor cells and metformin inhibits the effect through the mTOR signaling pathway

Author(s):  
Youji Feng



Renal Failure ◽  
2021 ◽  
Vol 43 (1) ◽  
pp. 1470-1478
Author(s):  
Suqing Li ◽  
Cong Qin ◽  
Yike Chen ◽  
Dan Wei ◽  
Zhijun Tan ◽  
...  


2021 ◽  
Vol 22 (6) ◽  
Author(s):  
Yuying Fan ◽  
Xiaoli Ren ◽  
Yingxue Wang ◽  
Enshuang Xu ◽  
Shuang Wang ◽  
...  


2015 ◽  
Vol 55 (11) ◽  
pp. 1688-1699 ◽  
Author(s):  
Qi Wang ◽  
Yong Tang ◽  
Hongjing Yu ◽  
Qiaoyun Yin ◽  
Mengdi Li ◽  
...  




2006 ◽  
Vol 4 (12) ◽  
pp. 181
Author(s):  
M. Breuleux ◽  
S. Zumstein-Mecker ◽  
T. O'Reilly ◽  
F. Natt ◽  
M. Maira ◽  
...  




2018 ◽  
Vol 10 (2) ◽  
pp. 215-222
Author(s):  
Yan-Er Wang ◽  
Kun Xu ◽  
Wen-Hua Yue ◽  
Qiong-Ming Xu ◽  
Ben-Gang You ◽  
...  


Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2129
Author(s):  
Daniel J. Smit ◽  
Laure Cayrefourcq ◽  
Marie-Therese Haider ◽  
Nico Hinz ◽  
Klaus Pantel ◽  
...  

Circulating tumor cells (CTCs) are cells shed from the primary tumor into the bloodstream. While many studies on solid tumor cells exist, data on CTCs are scarce. The mortality of cancer is mostly associated with metastasis and recent research identified CTCs as initiators of metastasis. The PI3K/AKT/mTOR signaling pathway is an intracellular pathway that regulates essential functions including protein biosynthesis, cell growth, cell cycle control, survival and migration. Importantly, activating oncogenic mutations and amplifications in this pathway are frequently observed in a wide variety of cancer entities, underlining the significance of this signaling pathway. In this study, we analyzed the functional role of the PI3K/AKT/mTOR signaling pathway in the CTC-MCC-41 line, derived from a patient with metastatic colorectal cancer. One striking finding in our study was the strong sensitivity of this CTC line against AKT inhibition using MK2206 and mTOR inhibition using RAD001 within the nanomolar range. This suggests that therapies targeting AKT and mTOR could have been beneficial for the patient from which the CTC line was isolated. Additionally, a dual targeting approach of AKT/mTOR inside the PI3K/AKT/mTOR signaling pathway in the colorectal CTCs showed synergistic effects in vitro. Depending on the phenotypical behavior of CTC-MCC-41 in cell culture (adherent vs. suspension), we identified altered phosphorylation levels inside the PI3K/AKT/mTOR pathway. We observed a downregulation of the PI3K/AKT/mTOR signaling pathway, but not of the RAS/RAF/MAPK pathway, in CTCs growing in suspension in comparison to adherent CTCs. Our results highlight distinct functions of AKT isoforms in CTC-MCC-41 cells with respect to cell proliferation. Knockdown of AKT1 and AKT2 leads to significantly impaired proliferation of CTC-MCC-41 cells in vitro. Therefore, our data demonstrate that the PI3K/AKT/mTOR signaling pathway plays a key role in the proliferation of CTC-MCC-41.



Sign in / Sign up

Export Citation Format

Share Document