MicroRNA-26a suppresses tumor growth and metastasis of human hepatocellular carcinoma by targeting interleukin-6-Stat3 pathway
Open accessAbstract
Down-regulation of microRNA-26a (miR-26a) is associated with poor prognosis of hepatocellular carcinoma (HCC), but its functional mechanism in HCC remains unclear. In this study, we investigated the roles of miR-26a in tumor growth and metastasis of HCC and found that miR-26a was frequently down-regulated in HCC tissues. Down-regulation of miR-26a correlated with HCC recurrence and metastasis. Through gain- and loss-of-function studies, miR-26a was demonstrated to significantly inhibit in vitro cell proliferation, migration, and invasion. In addition, miR-26a induced G1 arrest and promoted apoptosis of HCC cells. Importantly, miR-26a suppressed in vivo tumor growth and metastasis in nude mice models bearing human HCC. Interleukin-6 (IL-6) was identified as a target of miR-26a. Knockdown of IL-6 induced effects on HCC cells similar to those induced by miR-26a. In contrast, IL-6 treatment abrogated the effects induced by miR-26a up-regulation. Moreover, miR-26a dramatically suppressed expression of signal transducer and activator of transcription 3 (Stat3) target genes, including Bcl-2, Mcl-1, cyclin D1, and MMP2. IL-6 treatment antagonized this effect, while knockdown of IL-6 by IL-6 short hairpin RNA (shIL-6) induced inhibitory effects on the expression of p-Stat3 and its main target genes, similar to miR-26a. The messenger RNA and protein levels of IL-6 inversely correlated with miR-26a in HCCs. Patients with high miR-26a or low IL-6 in HCC tissues had a better prognosis with longer overall survival (OS) and time to recurrence (TTR). In multivariate analysis, miR-26a, IL-6, and their combination were demonstrated to be independent prognostic indicators for OS and TTR of HCC patients. Conclusion: miR-26a could suppress tumor growth and metastasis of HCC through IL-6-Stat3 signaling and is a novel prognostic marker and therapeutic target for HCC. (HEPATOLOGY 2013)
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The three selected miRNAs-hsa-miR-122-5p, hsa-let-7a-5p, and hsa-miR-26a-5p-provide complementary and comprehensive coverage of almost all critical genes associated with the MAPK signaling pathway.
“From this analysis, we selected the three abundant miRNAs-hsa-miR-122-5p, hsa-let-7a-5p, and hsa-miR26a-5p-based on their complementary and comprehensive coverage of almost all the critical genes associated with the MAPK signaling pathway 27-33 as analyzed using miRTarBase version 8.0 and TarBase v8.0 integrated within miRNet (Figure S1).”
From rAAV-mediated Multi-miRNA Delivery Targeting MAPK Pathway Suppresses Laser-induced Choroidal Neovascularization in Mice (2026) · cites this paper as [32]
The introductory passage labeled Abstract in our copy lists MAP3K2 among reported targets of miR-26a, supporting a limited connection between one selected miRNA and a MAPK-related gene. The paper's IL-6–Stat3 results do not assess the three miRNAs together or show that they cover almost all critical MAPK-pathway genes. (LLM, conf=0.83)
Experimental — accuracy not yet measuredmiR-26a-5p has anti-angiogenic properties and targets MAPK pathway components, including p38.
“hsa-miR-26a-5p is a well-documented tumor suppressor miRNA with anti-angiogenic properties 32 42,43 and have been shown to target components of the MAPK pathway, including p38.”
From rAAV-mediated Multi-miRNA Delivery Targeting MAPK Pathway Suppresses Laser-induced Choroidal Neovascularization in Mice (2026) · cites this paper as [32]
The introductory passage under the Abstract heading describes miR-26a as a tumor suppressor in several cancers and lists MAP3K2 among reported target mRNAs. The paper does not establish anti-angiogenic activity for miR-26a or identify p38 as a target; its mechanistic findings instead concern IL-6–Stat3 signaling (MiR-26a Inhibits the IL-6-Stat3 Signaling Pathway). Page numbers are unavailable in our copy. (LLM, conf=0.85)
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Self-citation
- Authors
- Yang, X., Liang, L., Zhang, X.-F., Jia, H.-L., Qin, Y., Zhu, X.-C., Gao, X.-M., Qiao, P., Zheng, Y., Sheng, Y.-Y., Wei, J.-W., Zhou, H.-J., Ren, N., Ye, Q.-H., Dong, Q.-Z., & Qin, L.-X.
- Affiliations
- Ministry of Education of the People's Republic of China (CN)
- Shanghai Medical College of Fudan University (CN)
- Corresponding author
- Qin, Lun-Xiu
- ORCID
- Venue
- Hepatology
- Published
- 2013-07
- Volume
- 58
- Issue
- 1
- Pages
- 158-170
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2072993593
- Cited by
- 280
- References
- 49
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 6 · 2023: 7 · 2022: 17 · 2021: 14 · 2020: 17 · 2019: 20 · 2018: 35 · 2017: 37 · 2016: 37 · 2015: 27 · 2014: 34 · 2013: 14
- FWCI
- 13.06
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Hepatology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Ministry of Education of the People's Republic of China
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- microRNA-26a, hepatocellular carcinoma, interleukin-6, STAT3 signaling, metastasis, tumor growth, prognostic factors, apoptosis, cell cycle arrest, Bcl-2, Mcl-1, cyclin D1, MMP-2, tumor recurrence, microRNA therapeutic target
- MeSH terms
- Animals, Female, Carcinoma, Hepatocellular, Humans, Liver Neoplasms, Male, Mice, Nude, Middle Aged, Signal Transduction, Down-Regulation, Interleukin-6, MicroRNAs, STAT3 Transcription Factor, Mice
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