scholarly journals YM155, a survivin suppressant, triggers PARP-dependent cell death (parthanatos) and inhibits esophageal squamous-cell carcinoma xenografts in mice

Oncotarget ◽  
2015 ◽  
Vol 6 (21) ◽  
pp. 18445-18459 ◽  
Author(s):  
Nan Zhao ◽  
Yousheng Mao ◽  
Gaijing Han ◽  
Qiang Ju ◽  
Lanping Zhou ◽  
...  
Esophagus ◽  
2018 ◽  
Vol 15 (2) ◽  
pp. 103-108 ◽  
Author(s):  
Yasunori Akutsu ◽  
Kentaro Murakami ◽  
Masayuki Kano ◽  
Takeshi Toyozumi ◽  
Yasunori Matsumoto ◽  
...  

Oncotarget ◽  
2016 ◽  
Vol 7 (35) ◽  
pp. 56758-56766 ◽  
Author(s):  
Bing-Li Wu ◽  
Dong Wang ◽  
Wen-Jing Bai ◽  
Fan Zhang ◽  
Xing Zhao ◽  
...  

2012 ◽  
Vol 72 (16) ◽  
pp. 3967-3976 ◽  
Author(s):  
Yoshiyuki Suzuki ◽  
Kousaku Mimura ◽  
Yuya Yoshimoto ◽  
Mitsuaki Watanabe ◽  
Yu Ohkubo ◽  
...  

Oncotarget ◽  
2016 ◽  
Vol 7 (16) ◽  
pp. 21542-21555 ◽  
Author(s):  
Wei Li ◽  
Guixue Hou ◽  
Dianrong Zhou ◽  
Xiaomin Lou ◽  
Yang Xu ◽  
...  

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Lei Guo ◽  
Ying Ji ◽  
Wei Guo ◽  
Peng Song ◽  
Xue-Min Xue ◽  
...  

Author(s):  
Huasong Liu ◽  
Jun Zhang ◽  
Xiangyu Luo ◽  
Min Zeng ◽  
Liqiang Xu ◽  
...  

Emerging evidence has demonstrated that long noncoding RNAs (lncRNAs) mediate the development of esophageal squamous cell carcinoma (ESCC) via various pathophysiological pathways. This study explored the impact of the lncRNA FOXD2-AS1 on cisplatin resistance in ESCC and its possible mechanisms. Upregulation of FOXD2-AS was detected in patients with ESCC and ESCC cells that are resistant to cisplatin. In an in vitro assay, knockdown of FOXD2-AS1 noticeably inhibited cell invasion and growth, triggered cell death, and repressed the stimulation of the Akt/mTOR axis in cisplatin-resistant ESCC cells (TE-1/DDP). Conversely, the overexpression of FOXD2-AS1 remarkably increased cell invasion and growth, repressed cell death, and triggered the stimulation of the Akt/mTOR axis in TE-1/DDP cells. These findings, along with bioinformatics and validation tests, showed that FOXD2-AS1 targeted miR-195 by acting as a competing endogenous RNA. FOXD2-AS1/miR-195/Akt/mTOR axis plays a crucial role in resistance to cisplatin in ESCC cells, offering an innovative strategy to treat ESCC.


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