Up-regulation of long noncoding RNA FALEC predicts poor prognosis and promotes melanoma cell proliferation through epigenetically silencing p21

被引:36
作者
Ni, Nana [1 ,2 ,3 ,4 ]
Song, Hao [1 ,2 ]
Wang, Xiaopo [1 ,2 ]
Xu, Xiulian [1 ,2 ]
Jiang, Yiqun [1 ,2 ]
Sun, Jianfang [1 ,2 ]
机构
[1] Chinese Acad Med Sci, Inst Dermatol, Dept Pathol, Nanjing 210042, Jiangsu, Peoples R China
[2] Peking Union Med Coll, Nanjing 210042, Jiangsu, Peoples R China
[3] Jiangsu Key Lab Mol Biol Skin Dis, Nanjing 210042, Jiangsu, Peoples R China
[4] STIs, Nanjing 210042, Jiangsu, Peoples R China
关键词
Melanoma; FALEC; EZH2; H3K27me3; p21; MALIGNANT-TRANSFORMATION; CANCER; EXPRESSION; TRANSITION; BMI1;
D O I
10.1016/j.biopha.2017.11.060
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Accumulating evidences have suggested that focally amplified lncRNA on chromosome 1 (FALEC) serves as an oncogenic long non-coding RNA (lncRNA) and has been identified to be dysregulated in various tumors. However, the expression, clinical values, and biological function of FALEC in melanoma are still unknown. In this study we detected the expression level of FALEC in tumor tissues and cell lines and measured the prognostic value of FALEC for melanoma patients and the biological effects of FALEC on melanoma cell proliferation, cell cycle, and apoptosis. Our results indicated that FALEC was more highly expressed in melanoma tissues and cell lines than in non-neoplastic nevi tissues and normal cell lines. Moreover, functional assays showed that silenced FALEC suppressed the proliferation of melanoma cells, resulted in cell cycle arrest, and induced apoptosis. Mechanically, we discovered that FALEC boosted melanoma progression via epigenetically repressing p21 through recruiting EZH2 to the promoter of p21. Generally, our results suggested that FALEC acted as an oncogene in melanoma and had the potential to be a prognostic biomarker and therapeutic target for melanoma.
引用
收藏
页码:1371 / 1379
页数:9
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