ArticleGene regulation and systems biology2014
Tetracycline derivative minocycline inhibits autophagy and inflammation in concanavalin-a-activated human hepatoma cells.
Article in Gene regulation and systems biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 17 citations in OpenAlex.
- Synthetic 1,3,6-Tri-O-Galloyl-α-D-Glucose Mimics the Hippo Pathway Inhibitor VT107 in Suppressing Concanavalin A-Induced Inflammation in Human Glioblastoma Cells.Journal of inflammation research · 2025Article
- P2YPurinergic signalling · 2022Article
- Concanavalin A as a promising lectin-based anti-cancer agent: the molecular mechanisms and therapeutic potential.Cell communication and signaling : CCS · 2022Review
- The Anticancer Potential of Doxycycline and Minocycline-A Comparative Study on Amelanotic Melanoma Cell Lines.International journal of molecular sciences · 2022Article
- MT1-MMP Cooperates with TGF-β Receptor-Mediated Signaling to Trigger SNAIL and Induce Epithelial-to-Mesenchymal-like Transition in U87 Glioblastoma Cells.International journal of molecular sciences · 2021Article
- Minocycline in Treating Glioblastoma Multiforme: Far beyond a Conventional Antibiotic.Journal of oncology · 2020Review
- Minocycline Induces Autophagy and Inhibits Cell Proliferation in LPS-Stimulated THP-1 Cells.BioMed research international · 2020Article
- Minocycline attenuates sevoflurane-induced cell injury via activation of Nrf2.International journal of molecular medicine · 2017Article
- A Transcriptional Regulatory Role for the Membrane Type-1 Matrix Metalloproteinase in Carcinogen-Induced Inflammasome Gene Expression.Gene regulation and systems biology · 2017Article
- Impact of Concanavalin-A-Mediated Cytoskeleton Disruption on Low-Density Lipoprotein Receptor-Related Protein-1 Internalization and Cell Surface Expression in Glioblastomas.Biomarkers in cancer · 2016Article
- Minocycline alleviates sevoflurane-induced cognitive impairment in aged rats.Cellular and molecular neurobiology · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of soluble matrix metalloproteinase (MMP) activity is among the non-antibiotic cellular effects exerted by the anti-inflammatory tetracycline derivative minocycline. The impact of minocycline on the signal transduction functions of membrane-bound MMPs is however unknown. We assessed minocycline in a concanavalin-A (ConA)-activated human HepG2 hepatoma cell model, a condition known to increase the expression of membrane type-1 MMP (MT-MMP) and to trigger inflammatory and autophagy processes. We found that minocycline inhibited ConA-induced formation of autophagic acidic vacuoles, green fluorescent microtubule-associated protein 1 light chain 3 (GFP-LC3) puncta formation, gene and protein expression of autophagy biomarker BCL2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3), invasion biomarker MT1-MMP, and inflammation biomarker cyclooxygenase (COX)-2. Gene silencing of MT1-MMP abrogated ConA-induced formation of autophagic acidic vacuoles and ConA-induced expressions of BNIP3 and COX-2. Minocycline was also shown to inhibit ConA-induced signal transducer and activator of transcription 3 (STAT3) phosphorylation as well as gene expression of NANOS1, a biomarker believed to colocalize with MT1-MMP and the specific silencing of which further inhibited ConA-induced STAT3 phosphorylation. Collectively, our data demonstrate that part of minocycline's effects on autophagy could be exerted through the inhibition of MT1-MMP signaling functions, which contribute to the autophagy and inflammatory phenotype of ConA-activated HepG2 cells.
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