Overexpression of the Long Noncoding RNA FOXD2-AS1 Promotes Cisplatin Resistance in Esophageal Squamous Cell Carcinoma Through the miR-195/Akt/mTOR Axis.

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.
Authors	Huasong Liu, Jun Zhang, Xiangyu Luo, Min Zeng, Liqiang Xu, Qunxian Zhang, Hua Liu, Jialong Guo, Lanlan Xu
Journal	Oncology research (Oncol Res) Vol. 28 Issue 1 Pg. 65-73 (Feb 07 2020) ISSN: 1555-3906 [Electronic] United States
PMID	31558183 (Publication Type: Journal Article)
Chemical References	FOXD2 protein, human Forkhead Transcription Factors MIRN195 microRNA, human MicroRNAs RNA, Long Noncoding long non-coding RNA FOXD2-AS1, human MTOR protein, human Proto-Oncogene Proteins c-akt TOR Serine-Threonine Kinases Cisplatin
Topics	Cell Line, Tumor Cell Proliferation (genetics) Cisplatin (pharmacology) Drug Resistance, Neoplasm (genetics) Esophageal Neoplasms (drug therapy, genetics, pathology) Esophageal Squamous Cell Carcinoma (drug therapy, genetics, pathology) Female Forkhead Transcription Factors (genetics, metabolism) Humans Male MicroRNAs (genetics, metabolism) Proto-Oncogene Proteins c-akt (genetics, metabolism) RNA, Long Noncoding (genetics) TOR Serine-Threonine Kinases (genetics, metabolism) Up-Regulation (genetics)

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