MicroRNA-34a inhibits esophageal squamous cell carcinoma progression by targeting E2F5

被引:2
作者
Jiang, Hong [1 ]
Guo, Yi [1 ]
Huang, Kanghua [1 ]
Lu, Rongxia [1 ]
Peng, Xiaohong [2 ]
Lin, Shaoxiong [3 ]
机构
[1] Shantou Univ, Med Coll, Canc Hosp, Endoscopy Ctr, Shantou 515041, Peoples R China
[2] Southern Med Univ, Nanfang Hosp, Dept Otorhinolaryngol Head & Neck Surg, Guangzhou 510000, Guangdong, Peoples R China
[3] Shantou Univ, Med Coll, Affiliated Hosp 1, Dept Otolaryngol, 57 Changping Rd, Shantou 515041, Guangdong, Peoples R China
来源
JOURNAL OF BUON | 2019年 / 24卷 / 06期
关键词
microRNA-34a; esophageal squamous cell carcinoma; E2F5; MESENCHYMAL TRANSITION; CYCLE ARREST; CANCER; METASTASIS; ACTIVATION; EXPRESSION; MIRNAS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Purpose: Previous studies have explored the role of microRNA-34a (miR-34a) and E2F transcription family in several tumors, however, the expression level and oncogenesis mechanism of these two factors in esophageal squamous cancer cells (ESCC) remains unclear. Our study aims to explore the inhibitory effect of miR-34a in ESCC as well as its downstream factor E2F5. Methods: We explored the relevant expression level of miR-34a in human tumor tissue as well as in several ESCC cell lines. Through RNA mimic and inhibitor, we examined the specific role of miR-34a in the proliferation, apoptosis and migration of tumor cells, and we further explored the role of downstream factor E2F5 through gain- and loss-of-function analyses. Results: We found that the expression level of miR-34a is significantly downregulated in ESCC tissues as well as in ESCC cell lines, and miR-34a plays an inhibitory role in tumor cell proliferation and migration while it promotes tumor cell apoptosis. We further showed that E2F5 is a direct functional target of miR-34a, as it promotes tumor cell proliferation and migration and inhibits apoptosis. Conclusions: Our results indicate that the intrinsic expression of miR-34a was relatively low in ESCC. The anti-tumor effect of miR-34a is possibly dependent on the regulation of cell-cycle regulator E2F5.
引用
收藏
页码:2514 / 2522
页数:9
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