Abstract
Aberrant expression of microRNAs (miRNAs) has been shown to be associated with the progression and metastasis of cancer. Dysregulation of miR‑144 has been observed in numerous types of cancer; however, the exact role of miR‑144 in hepatocellular carcinoma (HCC) remains unclear. The present study observed that miR‑144 was downregulated in HCC tissues and cell lines. Forced overexpression of miR‑144 suppressed proliferation, migration and invasion of HCC cells. AKT3 was identified as a direct target of miR‑144 in HCC, and this was confirmed by a luciferase activity assay and western blot analysis. Overexpression of AKT3 in miR‑144 transfected HCC cells effectively reversed the tumor suppressive effects of miR‑144. Furthermore, AKT3 expression levels were inversely correlated with miR‑144 expression levels in HCC tissues. In conclusion, the results of the present study suggest that miR‑144 may act as a tumor suppressor in HCC by targeting AKT3, and miR‑144 may be a potential therapeutic candidate for HCC.
Highlights
Introduction regulation of gene expressionmiRNAs bind to the 3'‐untranslated region (3'‐UTR) of genes by imperfect base‐pairing to complementary sequences, and induce target mRNA degradation or translational repression [4]
Concordant with the tissue results, miR‐144 was markedly downregulated in the hepatocellular carcinoma (HCC) cell lines, as compared with the normal hepatocytes (Fig. 1B)
To explore the function of miR‐144 in tumor proliferation, the SMMC‐7721 cells were transfected with miR‐144 or a control miRNA. miR‐144 overexpression significantly suppressed the proliferation of SMMC‐7721 cells, as determined by a Cell Counting kit‐8 (CCK‐8) assay (Fig. 2A)
Summary
MiRNAs bind to the 3'‐untranslated region (3'‐UTR) of genes by imperfect base‐pairing to complementary sequences, and induce target mRNA degradation or translational repression [4]. Emerging evidence has demonstrated the aberrant expression of miRNAs in numerous types of cancer, including HCC [5,6,7]. MiR‐144 is aberrantly expressed in various malignancies, including bladder [8], colorectal (CRC) [9] and lung cancer [10], as well as HCC [11]. There are various signaling pathways through which miR‐144 plays a critical role in the development of numerous cancers, by targeting different molecules involved in those signalling pathways. A number of these target molecules have been experimentally identified, including enhancer of zeste homolog 2 (EZH2), mammalian target of rapamycin (mTOR) and Zinc finger X‐chromosomal protein [8,9,10].
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