High MALAT1 expression predicts a poor prognosis of cervical cancer and promotes cancer cell growth and invasion

被引:7
|
作者
Yang, L. [1 ]
Bai, H. -S. [1 ,2 ]
Deng, Y. [1 ]
Fan, L. [3 ]
机构
[1] Univ Elect Sci & Technol China, Sch Clin Med, Sichuan Prov Peoples Hosp, Dept Oncol, Chengdu 610054, Peoples R China
[2] Zunyi Med Coll, Grad Sch, Zunyi, Peoples R China
[3] Sichuan Canc Hosp, Ctr Radiotherapy, Chengdu, Peoples R China
关键词
MALAT1; Prognosis; Cervical cancer; Growth; Invasion; NONCODING RNA MALAT1; UP-REGULATION; COLORECTAL-CANCER; PROLIFERATION; METASTASIS; PROGRESSION; CARCINOMA;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: Although the oncogenic role of long non-coding RNA, MALAT1 in cervical cancer is gradually recognized, the clinical and prognostic significance of this lncRNA in cervical cancer has not been reported yet. This study aimed to investigate the clinical significance and biological functions of MALAT1 in cervical cancer. PATIENTS AND METHODS: MALAT1 expression in 104 cervical cancer tissues and matched adjacent normal tissues, as well as in 50 HPV negative heathy cervical tissues were quantified using qRT-PCR. Its association with overall survival of the cancer patients was analyzed using the Log-rank (Mantel-Cox) test and the Cox proportional hazards model. In addition, the effect of MALAT1 on cell proliferation and invasion was further studied in Hela and CaSki cells. RESULTS: MALAT1 expression is significantly increased in cervical cancer than in normal tissues. Its expression in the cancerous tissues is also significantly higher than in adjacent normal tissues. MALAT1 expression is correlated with tumor size, FIGO stage, vascular invasion and lymph nodes metastasis and is an independent predictor for overall survival of cervical cancer. When endogenous MALAT1 was knocked down, the cancer cells had significantly reduced proliferation and invasion and increased apoptosis. CONCLUSIONS: MALAT1 might be an important marker of prognosis and a potential therapeutic target of cervical cancer.
引用
收藏
页码:3187 / 3193
页数:7
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