scholarly journals Surgery-induced wound response promotes stem-like and tumor-initiating features of breast cancer cells, via STAT3 signaling

Oncotarget ◽  
2014 ◽  
Vol 5 (15) ◽  
pp. 6267-6279 ◽  
Author(s):  
Ilenia Segatto ◽  
Stefania Berton ◽  
Maura Sonego ◽  
Samuele Massarut ◽  
Tiziana Perin ◽  
...  
RSC Advances ◽  
2017 ◽  
Vol 7 (29) ◽  
pp. 18085-18092 ◽  
Author(s):  
Shilong Ning ◽  
Xiao Ma ◽  
Dongmei Zhu ◽  
Zhaoxia Shen ◽  
Jiao Liu ◽  
...  

Activated STAT3 triggered miR-21 transcription via binding to its promoter. ISL induced PIAS3 expression, a specific inhibitor of activated STAT3, leading to inhibition of STAT3 signaling and subsequent miR-21 transcription in breast cancer cells.


PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e82821 ◽  
Author(s):  
Li Lin ◽  
Brian Hutzen ◽  
Hsiu-Fang Lee ◽  
Zhengang Peng ◽  
Wenlong Wang ◽  
...  

2019 ◽  
Vol 514 (3) ◽  
pp. 639-644 ◽  
Author(s):  
Wei-hao Lin ◽  
Wei-gang Dai ◽  
Xiang-dong Xu ◽  
Qiu-hua Yu ◽  
Bing Zhang ◽  
...  

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e14638-e14638
Author(s):  
Pei-Chen Hsu ◽  
Jar-Yi Ho ◽  
Cheng-Ping Yu

e14638 Background: Breast cancer is the highest incidence malignancies in women worldwide. Luminal breast cancers are typically estrogen receptor–positive with better prognosis. However, the rapid disease progression and the high relapse rate of this subtype of breast cancer have become a puzzle in breast cancer treatment. It gave us the motivation to figure out the anomalous molecular mechanism which devoted in. It has been well-documented that the RAS pathway is overloadly activated in more than half of human breast tumors. RAS genes encode a superfamily of small GTPases that contribute to cell growth signals. Methods: Gene expression level were measured by qPCR and Western Blot.Biological effects of each condition were evaluated in cell viability and migration. Results: In this study, we investigated one member of the RAS family, RERG, which was related to the ER pathway and contributed to inhibit Ras activated pathway. Our results showed that knockdown of RERG concomitantly promoted two major oncogenic pathways, Ras and Stat3 signaling pathways, in luminal type breast cancer cell lines. Moreover, ectopic RERG expression significantly inhibited Ras expression. It implicated that RERG mediated in RAS-driven biological effects. Our findings indicated that knockdown of RERG enhanced mobility of the breast cancer cells and made cells more intractable under SERM treatment. Conclusions: We elucidated the tumor-suppressor role of RERG in breast cancer cells though inhibition of the Ras and Stat3 signaling pathways. Therefore, this study might shed light on the important mechanistic insight into the tumorigenesis of ER-positive luminal type cancer and provided the prognostic and therapeutic improved roles of RERG.


2009 ◽  
Vol 31 (2) ◽  
pp. 192-200 ◽  
Author(s):  
R. Behera ◽  
V. Kumar ◽  
K. Lohite ◽  
S. Karnik ◽  
G. C. Kundu

Sign in / Sign up

Export Citation Format

Share Document