@Article{096504019X15656904013079,
AUTHOR = {Huasong Liu, Jun Zhang, Xiangyu Luo, Min Zeng, Liqiang Xu, Qunxian Zhang, Hua Liu, Jialong Guo, Lanlan Xu},
TITLE = {Overexpression of the Long Noncoding RNA FOXD2-AS1 Promotes  Cisplatin Resistance in Esophageal Squamous Cell Carcinoma  Through the miR-195/Akt/mTOR Axis},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {1},
PAGES = {65--73},
URL = {http://www.techscience.com/or/v28n1/48548},
ISSN = {1555-3906},
ABSTRACT = {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.},
DOI = {10.3727/096504019X15656904013079}
}