Long non-coding RNA FOXD2-AS1 aggravates nasopharyngeal carcinoma carcinogenesis by modulating miR-363-5p/S100A1 pathway

被引：59

作者：

Chen, Gang ^{[1
]}

Sun, Wenjie ^{[2
]}

Hua, Xinying ^{[1
]}

Zeng, Wei ^{[1
]}

Yang, Lijing ^{[1
]}

机构：

[1] Wuhan Univ, Zhongnan Hosp, Dept Radiat & Med Oncol, Wuhan 430071, Hubei, Peoples R China

[2] Hubei Biopharmaceut Ind Technol Inst Inc, East Lake High Tech Dev Zone, 666 Gaoxin Rd, Wuhan 430075, Hubei, Peoples R China

来源：

GENE | 2018年 / 645卷

关键词：

FOXD2-AS1; miR-363-5p; S100A1; Nasopharyngeal carcinoma (NPC); Tumorigenesis; CELL LUNG-CANCER; DOWN-REGULATION; HEPATOCELLULAR-CARCINOMA; MDX MICE; COLORECTAL-CANCER; S100A1; EXPRESSION; C-MYC; PROLIFERATION; PROGRESSION; METASTASIS;

D O I：

10.1016/j.gene.2017.12.026

中图分类号：

Q3 [遗传学];

学科分类号：

071007 [遗传学];

摘要：

Long non-coding RNAs (IncRNAs) have been wildly verified to modulate multiple tumorigenesis, especially nasopharyngeal carcinoma (NPC). In present study, we aim to investigate the role of IncRNA FOXD2-AS1 in the NPC carcinogenesis. It was indicated that FOXD2-AS1 was markedly increased in NPC tissues and cells in comparison to their corresponding controls. Moreover, the aberrant overexpression of FOXD2-AS1 indicated the poor prognosis of NPC patients. Silence of FOXD2-AS1 was able to repress NPC cell growth in vitro while overexpression of FOXD2-AS1 inversed this process. Moreover, in vivo tumor xenografts were established using CNE-1/SUNE-1 cells to investigate the function of FOXD2-AS1 in NSCLC tumorigenesis. Rescue assay was performed to further confirm that FOXD2-AS1 contributed to NPC progression by regulating miR-363-5p/S100A1 signal pathway. Taken together, our study discovered the oncogenic role of FOXD2-AS1 in clinical specimens and cellular experiments, showing the potential FOXD2-AS1/miR-363-5p/S100A1 pathway. This results and findings provide a novel insight for NPC tumorigenesis.

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页码：76 / 84

页数：9

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