Open Access

ARTICLE

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

Huasong Liu^*1, Jun Zhang^*1, Xiangyu Luo^*, Min Zeng^*, Liqiang Xu^*, Qunxian Zhang^*, Hua Liu^*, Jialong Guo^*, Lanlan Xu^†

* Department of Cardiothoracic Surgery, Taihe Hospital Affiliated to Hubei University of Medicine, Shiyan, Hubei, P.R. China
† Hubei University of Medicine, Hubei, P.R. China

Oncology Research 2020, 28(1), 65-73. https://doi.org/10.3727/096504019X15656904013079

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.

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Keywords

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