ArticlePloS one2013
Polo-like kinase 1 (PLK1) is involved in toll-like receptor (TLR)-mediated TNF-α production in monocytic THP-1 cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- A comprehensive analysis of epigenetic mechanisms regulating inflammation-induced TNF-α gene expression by small-molecule inhibitor screening.Molecular biology reports · 2026Article
- Functional RNAi Screening Identifies G2/M and Kinetochore Components as Modulators of TNFα/NF-κB Prosurvival Signaling in Head and Neck Squamous Cell Carcinoma.Cancer research communications · 2024Article
- PLK1 inhibition dampens NLRP3 inflammasome-elicited response in inflammatory disease models.The Journal of clinical investigation · 2023Article
- microRNAs: Critical Players during Helminth Infections.Microorganisms · 2022Review
- Identification of polo-like kinase 1 as a therapeutic target in murine lupus.Clinical & translational immunology · 2022Article
- Review
- Rigosertib inhibits MEK1-ERK pathway and alleviates lipopolysaccharide-induced sepsis.Immunity, inflammation and disease · 2021Article
- Thiophene-Based Compounds with Potential Anti-Inflammatory Activity.Pharmaceuticals (Basel, Switzerland) · 2021Review
- A novel role for C-C motif chemokine receptor 2 during infection with hypervirulent Mycobacterium tuberculosis.Mucosal immunology · 2018Article
- Ancylostoma ceylanicum infective third-stage larvae are activated by co-culture with HT-29-MTX intestinal epithelial cells.Parasites & vectors · 2017Article
- Targeting polo-like kinase 1 suppresses essential functions of alloreactive T cells.Immunologic research · 2016Article
- Age-related changes in monocytes exacerbate neointimal hyperplasia after vascular injury.Oncotarget · 2015Article
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo-like kinases (PLKs) have been reported to be essential components of anti-viral pathways. However, the role of PLKs in the production of pro-inflammatory cytokines induced by TLR activation is uncertain. We report here that monocytic THP-1 cells expressed PLK1, PLK2, PLK3 and PLK4. When THP-1 cells were treated with GW843682X, an inhibitor of PLK1 and PLK3, the results showed that GW843682X down-regulated Pam3CSK4- and LPS-induced TNF-α at both the gene and protein levels. GW843682X did not impact Pam3CSK4-induced IL-1β and IL-8 or LPS-induced IL-1β, but it down-regulated LPS-induced IL-8 significantly. Moreover, western blot results showed that TLRs activated PLK1, and PLK1 inhibition by RNA interference down-regulated Pam3CSK4-induced TNF-α production, suggesting the involvement of PLK1 in TNF-α up-regulation. In addition, GW843682X treatment for 12 to 24 h induced cell death and down-regulated MyD88, but neither of these roles contributed to the down-regulation of TNF-α, as TNF-α gene expression was up-regulated at 1 h. Furthermore, GW843682X inhibited Pam3CSK4-induced activation of ERK and NF-κB, which contributed to Pam3CSK4-induced up-regulation of TNF-α. GW843682X also inhibited LPS-induced activation of ERK, p38 and NF-κB, which contributed to LPS-induced up-regulation of TNF-α. Taken together, these results suggested that PLK1 is involved in TLR2- and TLR4-induced inflammation, and GW843682X may be valuable for the regulation of the inflammatory response.
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