SALL4 and microRNA: The Role of Let-7

被引:11
作者
Liu, Jun [1 ]
Sauer, Madeline A. [1 ]
Hussein, Shaza G. [2 ]
Yang, Junyu [1 ]
Tenen, Daniel G. [3 ,4 ]
Chai, Li [1 ]
机构
[1] Brigham & Womens Hosp, Dept Pathol, 75 Francis St, Boston, MA 02115 USA
[2] Harvard Univ, Cambridge, MA 02138 USA
[3] Natl Univ Singapore, Canc Sci Inst, Singapore 117599, Singapore
[4] Harvard Med Sch, Harvard Stem Cell Inst, Boston, MA 02115 USA
基金
英国医学研究理事会;
关键词
SALL4; Let-7; LIN28; microRNA; miR-98; non-small cell lung cancer (NSCLC); hepatocellular carcinoma (HCC); CARCINOMA CELL-PROLIFERATION; UP-REGULATION; SUPPRESSIVE ROLE; LUNG-CANCER; EXPRESSION; INVASION; GLIOMA; APOPTOSIS; MIGRATION; DELIVERY;
D O I
10.3390/genes12091301
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
SALL4 is a zinc finger transcription factor that belongs to the spalt-like (SALL) gene family. It plays important roles in the maintenance of self-renewal and pluripotency of embryonic stem cells, and its expression is repressed in most adult organs. SALL4 re-expression has been observed in different types of human cancers, and dysregulation of SALL4 contributes to the pathogenesis, metastasis, and even drug resistance of multiple cancer types. Surprisingly, little is known regarding how SALL4 expression is controlled, but recently microRNAs (miRNAs) have emerged as important regulators of SALL4. Due to the ability of regulating targets differentially in specific tissues, and recent advances in systemic and organ specific miRNA delivery mechanisms, miRNAs have emerged as promising therapeutic targets for cancer treatment. In this review, we summarize current knowledge of the interaction between SALL4 and miRNAs in mammalian development and cancer, paying particular attention to the emerging roles of the Let-7/Lin28 axis. In addition, we discuss the therapeutic prospects of targeting SALL4 using miRNA-based strategies, with a focus on the Let-7/LIN28 axis.
引用
收藏
页数:14
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