Hepatitis B virus promotes cancer cell migration by downregulating miR-340-5p expression to induce STAT3 overexpression
Open accessAbstract
Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide, and infection with hepatitis B virus (HBV) is a leading cause of HCC. Previous studies have demonstrated that expression of the tumor inhibitor miR-340 is significantly downregulated in HCC tissues compared with normal liver tissues. However, the precise biological role of miR-340-5p in HBV–HCC and its molecular mechanism of action remain unknown. Expression of miR-340-5p was downregulated in HBV-associated HCC liver tissue and HBV-infected cells, facilitating migration of liver cancer cells. Signal transducer and activator of transcription (STAT)3 was found to be a direct functional target of miR-340-5p. The regulation of STAT3 expression by miR-340-5p was assessed using qRT-PCR and western blotting, and the effects of exogenous miR-340-5p and STAT3 on the migration of HBV-infected cells were evaluated in vitro using Transwell ® and wound-healing assays. The expression of E-cadherin and vimentin, associated with epithelial–mesenchymal transition, was also assessed using Western blotting after transfection of miR-340-5p mimics and/or STAT3 expression vectors. Overexpression of STAT3 resulted in rescue of HBV effects, decreased E-cadherin expression, increased vimentin expression, and ultimately, enhanced cell migration. Re-introduction of the STAT3 CDS led to marked reversal of the inhibition of cell migration in HBV-infected cells mediated by miR-340-5p. Hepatitis B virus promotes the migration of liver cancer cells by downregulating miR-340-5p expression to induce STAT3 overexpression. Our results show that STAT3 plays a key role in regulating cell migration in HBV–HCC involving miR-340-5p.
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Hepatitis B and hepatitis C viruses, which induce hepatitis and cause hepatocellular carcinoma, activate STAT3.
“Both hepatitis B and hepatitis C viruses, which induce hepatitis and cause hepatocellular carcinoma, activate STAT3 (328–330), while HTLV-I, Epstein–Barr virus and papilloma virus activate STAT3 and NF-κB (311, 331, 332).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [330]
The Background (page unavailable) associates both HBV and HCV infection with hepatocellular carcinoma. The Results (page unavailable) report that HBV increases STAT3 expression and that phosphorylated STAT3 follows the same trend. The paper does not report HCV activating STAT3 or establish that either virus induces hepatitis. (LLM, conf=0.88)
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Background
- Authors
- Xiong, Q., Wu, S., Wang, J., Zeng, X., Chen, J., Wei, M., Guan, H., Fan, C., Chen, L., Guo, D., & Sun, G.
- Affiliations
- Wuhan University (CN)
- Corresponding author
- Chen, Lang
- Guo, Deyin
- Sun, Guihong
- Venue
- Cell & Bioscience
- Published
- 2017-04-12
- Volume
- 7
- Issue
- 1
- Pages
- 16-16
- ISSN
- 2045-3701 (ISSN-L)
- PMC
- PMC5389182
- OpenAlex
- W2606953479
- Cited by
- 36
- References
- 24
- Citations by year
- 2025: 1 · 2024: 4 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 14 · 2019: 4 · 2018: 6
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Cell & Bioscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (81572447, 31570762, 31370187)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Epidemiology › Hepatitis B Virus Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- hepatitis B virus, hepatocellular carcinoma, miR-340-5p, STAT3, cell migration, epithelial-mesenchymal transition, E-cadherin, vimentin, microRNA downregulation, HBV-related liver cancer
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