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Updated: Apr 27, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Decrease expression of microRNA-744 promotes cell proliferation by targeting c-Myc in human hepatocellular carcinoma
Feng Lin1, Ruliang Ding1, Shuang Zheng1
1Department of General Surgery, Taizhou First People's Hospital, Taizhou, Zhejiang Province 318020, P.R. China.
Background:
MicroRNAs (miRNAs) are a large group of post-transcriptional gene regulators that potentially play a critical role in tumorigenesis. Increasing evidences indicate that miR-744 deregulated in numerous human cancers including hepatocellular carcinoma (HCC). However, its role in HCC carcinogenesis remains poorly defined. In this study, we investigated the roles of miR-744 in tumor growth of HCC.
Methods:
Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was conducted to detect the expression of miR-744 and Immunohistochemistry was performed to detect expression of c-Myc in HCC specimens and adjacent normal tissues. The biological functions of miR-744 were determined by cell proliferation and cell cycle assay. Furthermore, cell lines transfected with miR-744 mimics were analyzed in vitro. Luciferase reporter assays was performed to confirm whether miR-744 regulated the expression of c-Myc.
Results:
Our results showed that the expression of miR-744 was frequently down-regulated in both HCC tissues and cells. Furthermore, restoration of miR-744 in HCC cells was statistically correlated with decrease of cell growth and restored G1 accumulation. Luciferase assay and Western blot analysis revealed that c-Myc is a direct target of miR-744. Down-regulation of miR-744 and up-regulation of c-Myc were detected in HCC specimens compared with adjacent normal tissues. Moreover, restoration of miR-744 rescues c-Myc induced HCC proliferation.
Conclusions:
Our data suggest that miR-744 exerts its tumor suppressor function by targeting c-Myc, leading to the inhibition of HCC cell growth. miR-744 may serve as a potentially useful target for the miRNA-based therapies of HCC in the future.
Insights
MicroRNA 744 (miR-744) acts as a tumor suppressor in hepatocellular carcinoma (HCC) by inhibiting cell growth. Restoring miR-744 levels can reduce HCC proliferation by targeting c-Myc.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are key post-transcriptional regulators implicated in cancer.
- miR-744 is frequently deregulated in various cancers, including hepatocellular carcinoma (HCC).
- The precise role of miR-744 in HCC development is not fully understood.
Purpose of the Study:
- To investigate the function of miR-744 in HCC tumor growth.
- To determine the molecular mechanisms underlying miR-744's role in HCC.
Main Methods:
- Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) for miR-744 expression.
- Immunohistochemistry for c-Myc protein.
- Cell proliferation and cell cycle assays.
- Luciferase reporter assays to validate miR-744 targeting of c-Myc.
Main Results:
- miR-744 expression was significantly downregulated in HCC tissues and cells.
- Restoring miR-744 inhibited HCC cell proliferation and induced G1 cell cycle arrest.
- c-Myc was identified as a direct target of miR-744.
- Downregulation of miR-744 and upregulation of c-Myc were observed in HCC specimens.
Conclusions:
- miR-744 functions as a tumor suppressor in HCC by targeting c-Myc.
- Inhibition of HCC cell growth by miR-744 is mediated through c-Myc regulation.
- miR-744 holds potential as a therapeutic target for miRNA-based HCC treatments.
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