Targeting and neutralizing human epididymis protein 4 by novel nanobodies to suppress ovarian cancer cells and attenuate cisplatin resistance

Author(s):  
Jianli Yu ◽  
Yang Guo ◽  
Yi Gu ◽  
Fei Li ◽  
Haipeng Song ◽  
...  
2004 ◽  
Vol 92 (3) ◽  
pp. 896-904 ◽  
Author(s):  
Nicholas B Berry ◽  
Yong Mee Cho ◽  
Maureen A Harrington ◽  
Stephen D Williams ◽  
John Foley ◽  
...  

2014 ◽  
Vol 13 (1) ◽  
pp. 243 ◽  
Author(s):  
Huiyu Zhuang ◽  
Mingzi Tan ◽  
Juanjuan Liu ◽  
Zhenhua Hu ◽  
Dawo Liu ◽  
...  

Author(s):  
Yu-Jie Dong ◽  
Wei Feng ◽  
Yan Li

Ovarian cancer is a deadly gynecological malignancy with resistance to cisplatin a major clinical problem. We evaluated a role of long non-coding (lnc) RNA HOTTIP (HOXA transcript at the distal tip) in the cisplatin resistance of ovarian cancer cells, using paired cisplatin sensitive and resistant A2780 cells along with the SK-OV-3 cells. HOTTIP was significantly elevated in cisplatin resistant cells and its silencing reversed the cisplatin resistance of resistant cells. HOTTIP was found to sponge miR-205 and therefore HOTTIP silenced cells had higher levels of miR-205. Downregulation of miR-205 could attenuate HOTTIP-silencing effects whereas miR-205 upregulation in resistant cells was found to re-sensitize cells to cisplatin. HOTTIP silencing also led to reduced NF-κB activation, clonogenic potential and the reduced expression of stem cell markers SOX2, OCT4, and NANOG, an effect that could be attenuated by miR-205. Finally, ZEB2 was identified as the gene target of miR-205, thus completing the elucidation of HOTTIP-miR-205-ZEB2 as the novel axis which is functionally involved in the determination of cisplatin resistance in ovarian cancer cells.


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