Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates renal cancer cell migration via cofilin-1

被引:5
作者
Zhang, Yali [1 ,2 ]
Guan, Xinyu [1 ,2 ]
Wang, Hao [1 ,2 ]
Wang, Yong [3 ]
Yue, Dan [4 ]
Chen, Ruibing [2 ]
机构
[1] Tianjin Med Univ, Sch Basic Med Sci, Dept Genet, Tianjin 300070, Peoples R China
[2] Tianjin Univ, Sch Pharmaceut Sci & Technol, Hlth Sci Platform, 92 Weijin Rd, Tianjin 300072, Peoples R China
[3] Tianjin Med Univ, Hosp 2, Tianjin Inst Urol, Tianjin 300070, Peoples R China
[4] Tianjin Med Univ, Sch Med Lab, Tianjin 300070, Peoples R China
基金
中国国家自然科学基金;
关键词
lncRNA; MALAT1; RCC; CFL1; cell migration; cytoskeleton; UP-REGULATION; MALAT1; CARCINOMA; EXPRESSION; INTERACTS; REVEALS; TUMORS;
D O I
10.3892/ol.2020.11914
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is upregulated in numerous types of cancer, and is implicated in various cellular processes associated with cancer progression. However, the underlying molecular mechanisms by which MALAT1 regulates metastasis remain unclear. The present study investigated the expression of MALAT1 across a range of different cancer types by analyzing RNA sequencing data from The Cancer Genome Atlas database. The results indicate that the expression of MALAT1 is highly tissue-dependent and that MALAT1 is significantly overexpressed in renal clear cell carcinoma (KIRC). The biological role of MALAT1 in regulating KIRC cell migration was further investigated using molecular and cellular assays. The results demonstrate that MALAT1 regulates the expression of cofilin-1 (CFL1), potentially by regulating RNA splicing. MALAT1 knockdown decreased the expression of CFL1 at both the mRNA and protein levels, and affected cytoskeletal rearrangement by regulating the levels of F-actin via CFL1, leading to significantly decreased cellular migration. Clinical analysis confirmed a significant correlation between MALAT1 and CFL1 expression, implicating both genes as biomarkers for poor prognosis in KIRC. The present study demonstrates a novel mechanism by which MALAT1 regulates cell migration, which may be exploited to develop novel therapeutic strategies for managing renal cancer metastasis.
引用
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页数:11
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