Abstract
MicroRNAs (miRNAs) are dysregulated in many types of malignancies, including human hepatocellular carcinoma (HCC). MiR-107 has been implicated in several types of cancer regulation; however, relatively little is known about miR-107 in human HCC. In the present study, we showed that the overexpression of miR-107 accelerates the tumor progression of HCC in vitro and in vivo through its new target gene, CPEB3. Furthermore, our results demonstrated that CPEB3 is a newly discovered tumor suppressor that acts via the EGFR pathway. Therefore, our study demonstrates that the newly discovered miR-107/CPEB3/EGFR axis plays an important role in HCC progression and might represent a new potential therapeutic target for HCC treatment.
Highlights
Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies and a leading cause of cancer mortality worldwide [1,2,3,4]
We showed that miR-107 promotes the progression of HCC by targeting the Cytoplasmic polyadenylation element binding protein 3 (CPEB3)/epidermal growth factor receptor (EGFR) axis and that this newly discovered mechanism might provide a new potential therapeutic target for HCC treatment
To investigate the biological function of miR-107 in HCC progression, we performed MTT assays with two human HCC cell lines (HepG2 and Huh7) that were transfected with a miR-107 mimic and its negative control (NC mimic)(Figure 1A)
Summary
Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies and a leading cause of cancer mortality worldwide [1,2,3,4]. Several studies have identified a few genes that are involved in the progression of this malignancy, the pathogenesis of HCC remains to be elucidated [5, 6]. MiRNAs are a class of 17–24-bases non-coding RNA molecules that have become widely characterized as a critical regulator in the development and progression of cancer [7,8,9,10]. Recent studies have shown that speci fic miRNAs could have important influence on hepatic carcinogenesis and directly contribute to cell proliferation and metastasis in HCC [11,12,13]. We demonstrated that the overexpression of miR-107 promotes human HCC cell proliferation, migration and invasion
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