ArticleExperimental and therapeutic medicine2021
IL-17 promotes proliferation, inflammation and inhibits apoptosis of HaCaT cells via interacting with the TRAF3 interacting protein 2.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Olive (Olea europaea) phenolics for the control of psoriasis via targeting SMYD2 and IL-17A protein-protein interaction networks.Journal of natural medicines · 2026Article
- Astilbin Alleviates IL-17-Induced Hyperproliferation and Inflammation in HaCaT Cells via Inhibiting Ferroptosis Through the cGAS-STING Pathway.International journal of molecular sciences · 2025Article
- Discovery of PANoptosis-related signatures correlates with immune cell infiltration in psoriasis.PloS one · 2024Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the effects of interleukin-17 (IL-17) on the function of keratinocytes and to further investigate its associated mechanism. Human immortalized epidermal cells (HaCaT) were divided into sham control group (Sham), TRAF3 interacting protein 2 (TRAF3IP2)-knockdown with lentivirus group (si-TRAF3IP2), sham control+IL-17 group (Sham+IL-17) and TRAF3IP2-knockdown with lentivirus+IL-17 group (si-TRAF3IP2+IL-17). MTT and flow cytometry assays demonstrated that IL-17 promoted proliferation and inhibited apoptosis of HaCaT cells, while this effect was reversed following knockdown of TRAF3IP2 with lentiviral vectors. In addition, a marked increase in the levels of IL-6, IL-8, IL-23, TNF-α and VEGF was observed in the Sham+IL-17 group compared with that noted in the Sham group (P<0.05). Furthermore, reverse transcription-quantitative polymerase chain reaction and western blotting indicated that the mRNA and protein expression levels of caspase-3 in the si-TRAF3IP2+IL-17 group were significantly increased compared with those of the Sham+IL-17 group (P<0.05). Taken together, the results indicated that IL-17 promoted proliferation and inflammation and inhibited apoptosis of HaCaT cells by interacting with the TRAF3IP2 adaptor protein, while knockdown of the expression of TRAF3IP2 reduced the effects of IL-17 in HaCaT cells.
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