Long non-coding RNA highly up-regulated in liver cancer promotes epithelial-to-mesenchymal transition process in oral squamous cell carcinoma

被引:16
作者
Su, Wen [1 ,2 ]
Tang, Jing [3 ]
Wang, Yufan [1 ]
Sun, Shuai [1 ]
Shen, Yuehong [1 ]
Yang, Hongyu [1 ]
机构
[1] Peking Univ, Shenzhen Hosp, Dept Oral & Maxillofacial Surg, Shenzhen, Guangdong, Peoples R China
[2] Anhui Med Univ, Peking Univ, Shenzhen Hosp, Clin Coll, Hefei, Anhui, Peoples R China
[3] Jingzhou Cent Hosp, Jingzhou, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
epithelial-to-mesenchymal transition; highly up-regulated in liver cancer; long non-coding RNA; oral squamous cell carcinoma; HULC; PROGRESSION; CAVITY; PROLIFERATION; METASTASIS; EXPRESSION; APOPTOSIS; PROTEIN;
D O I
10.1111/jcmm.14160
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oral squamous cell carcinoma (OSCC) is an oral and maxillofacial malignancy that exhibits high incidence worldwide. In diverse human cancers, the long non-coding RNA (lncRNA) highly up-regulated in liver cancer (HULC) is aberrantly expressed, but how HULC affects OSCC development and progression has remained mostly unknown. We report that HULC was abnormally up-regulated in oral cancer tissues and OSCC cell lines, and that suppression of HULC expression in OSCC cells not only inhibited the proliferation, drug tolerance, migration and invasion of the cancer cells, but also increased their apoptosis rate. Notably, in a mouse xenograft model, HULC depletion reduced tumorigenicity and inhibited the epithelial-to-mesenchymal transition process. Collectively, our findings reveal a crucial role of the lncRNA HULC in regulating oral cancer carcinogenesis and tumour progression, and thus suggest that HULC could serve as a novel therapeutic target for OSCC.
引用
收藏
页码:2645 / 2655
页数:11
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