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Updated: Mar 1, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-30e acts as a tumor suppressor in hepatocellular carcinoma partly via JAK1/STAT3 pathway
Junjie Mao1, Xiaojun Hu1, Pengfei Pang1
1Center for Interventional Medicine, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong 519000, P.R. China.
Abstract:
Hepatocellular carcinoma (HCC) is the leading cause of cancer-associated mortalities. The effective diagnostic and therapeutic targets for HCC are still unclear. miR-30e was differentially expressed in the majority of HCC tissues and cell lines. The aim of this study was to investigate the functional roles of miR-30e and their modulation of cancer networks in HCC cells. We determined the expression of miR-30e by quantitative real-time polymerase chain reaction, and found downregulation of miR-30e in HepG2 and HuH7 cells. miR-30e mimics significantly inhibited the proliferation, migration, and invasion of HepG2 and HuH7 cells, and promoted cell apoptosis, but did not influence the cell cycle. Dual-luciferase reporter assays were applied to identify JAK1 as target of miR-30e. miR-30e mimics downregulated the expression levels of JAK1 and vimentin in mRNA and protein in HepG2 and HuH7 cells. Silence of JAK1 by small interfering RNAs inhibited cell proliferation, migration and invasion of HCC cells. Furthermore, we verified that, IL-6, an agonist of JAK1/STAT3 pathway partly recovered the inhibition of miR-30e mimics on cell migration. Taken together, these findings confirmed our speculation that the functional effect of miR-30e on HCC cells, in part, is dependent on the JAK1/STAT3 signaling pathway. It was suggested that miR-30e has a critical role in the suppression of HCC and presents a novel mechanism of miRNA-mediated JAK1 expression in cancer cells that might be a good prognostic marker for survival of HCC patients.
Insights
MicroRNA-30e (miR-30e) acts as a tumor suppressor in hepatocellular carcinoma (HCC) by inhibiting cell growth and invasion. This study identifies miR-30e as a novel therapeutic target in HCC, potentially improving patient survival.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality with unclear diagnostic and therapeutic targets.
- MicroRNA-30e (miR-30e) shows differential expression in HCC tissues and cell lines, suggesting a potential role.
Purpose of the Study:
- To investigate the functional roles of miR-30e in hepatocellular carcinoma (HCC) cells.
- To elucidate the underlying molecular mechanisms and cancer networks modulated by miR-30e.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) to determine miR-30e expression.
- Cell proliferation, migration, invasion, and apoptosis assays.
- Dual-luciferase reporter assays to identify miR-30e targets.
- Western blotting and small interfering RNA (siRNA) to assess gene silencing.
- Interleukin-6 (IL-6) treatment to investigate pathway modulation.
Main Results:
- miR-30e was downregulated in HCC cell lines (HepG2, HuH7).
- miR-30e mimics suppressed proliferation, migration, and invasion, and promoted apoptosis in HCC cells.
- JAK1 was identified as a direct target of miR-30e, with miR-30e mimics downregulating JAK1 expression.
- JAK1 silencing inhibited HCC cell proliferation, migration, and invasion.
- The JAK1/STAT3 pathway was implicated, as IL-6 partially reversed miR-30e mimic-induced inhibition of cell migration.
Conclusions:
- miR-30e functions as a tumor suppressor in HCC by targeting JAK1 and modulating the JAK1/STAT3 pathway.
- miR-30e represents a novel therapeutic target and potential prognostic biomarker for HCC.
- This study reveals a new mechanism of miRNA-mediated gene regulation in cancer cells.
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