Long intergenic non-coding RNA 00337 confers progression of esophageal cancer by mediating microrna-145-dependent fscn1

被引:7
|
作者
Shi, Lixia [1 ]
Chen, Qing [1 ]
Ge, Xiaofen [2 ]
机构
[1] Linyi Peoples Hosp, Dept Gen Surg, Linyi, Shandong, Peoples R China
[2] Linyi Peoples Hosp, Infect Dis Clin, 27 East Sect Jiefang Rd, Linyi 276000, Shandong, Peoples R China
关键词
esophageal cancer; FSCN1; invasion; long intergenic non-coding RNA; microRNA-145; migration; proliferation; SQUAMOUS-CELL CARCINOMA; EXPRESSION; PROLIFERATION; MIR-145; INVASION; ASSOCIATION; METASTASIS; MIGRATION; EPIDEMIOLOGY; HOTAIR;
D O I
10.1096/fj.202000470
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Long non-coding RNAs (lncRNAs) have been highlighted as prominent genetic modulators involved in multiple important biological processes of cancer cells, especially in esophageal cancer (EC). We tried to elucidate the potential role of LINC00337 in the progression of EC. Based on TCGA database analysis and Reverse transcription quantitative polymerase chain reaction determination, high expression of LINC00337 and FSCN1 was detected, while miR-145 exhibited a low expression in EC. LINC00337 was identified to bind to miR-145 to impair the miR-145-dependent FSCN1 inhibition. The underlying regulatory mechanisms were evaluated by transfection with LINC00337 overexpression plasmid, siRNA against LINC00337, miR-145 mimic, or anta-miR-145. Downregulation of LINC00337 results in increased Bax level, decreased FSCN1, Bcl-2, VEGF, and p53 levels, in addition to diminished cell proliferation, migration, invasion and tumor growth, with accelerated cell apoptosis by upregulating miR-145. Taken together, the findings obtained provided evidence suggesting that LINC00337 acts as a tumor promoter in EC, providing insight and advancements for EC treatment.
引用
收藏
页码:11431 / 11443
页数:13
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