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Doxycycline attenuates cancer cell growth by suppressing NLRP3-mediated inflammation

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dc.contributor.authorAlsaadi, Mohammad
dc.contributor.authorTezcan, Gülçin
dc.contributor.authorGaranina, Ekaterina E.
dc.contributor.authorHamza, Shaimaa
dc.contributor.authorMcIntyre, Alan
dc.contributor.authorRizvanov, Albert A.
dc.contributor.authorKhaiboullina, Svetlana F.
dc.contributor.buuauthorTEZCAN, GÜLÇİN
dc.contributor.departmentBursa Uludağ Üniversitesi/Diş Hekimliği Fakültesi/Temel Bilimler Bölümü.
dc.contributor.orcid0000-0002-5956-8755
dc.contributor.researcheridAAH-3843-2020
dc.date.accessioned2024-06-14T13:02:52Z
dc.date.available2024-06-14T13:02:52Z
dc.date.issued2021-08-24
dc.description.abstractNLR family pyrin domain containing 3 (NLRP3) inflammasome formation is triggered by the damaged mitochondria releasing reactive oxygen species. Doxycycline was shown to regulate inflammation; however, its effect on NLRP3 in cancer remains largely unknown. Therefore, we sought to determine the effect of doxycycline on NLRP3 regulation in cancer using an in vitro model. NLRP3 was activated in a prostate cancer cell line (PC3) and a lung cancer cell line (A549) before treatment with doxycycline. Inflammasome activation was assessed by analyzing RNA expression of NLRP3, Pro-CASP-1, and Pro-IL1 beta using RT-qPCR. Additionally, NLPR3 protein expression and IL-1 beta secretion were analyzed using Western blot and ELISA, respectively. Tumor cell viability was determined using Annexin V staining and a cell proliferation assay. Cytokine secretion was analyzed using a 41Plex assay for human cytokines. Data were analyzed using one-way ANOVA model with Tukey's post hoc tests. Doxycycline treatment decreased NLRP3 formation in PC3 and A549 cells compared to untreated and LPS only treated cells (p < 0.05). Doxycycline also decreased proliferation and caused cell death through apoptosis, a response that differed to the LPS-Nigericin mediated pyroptosis. Our findings suggest that doxycycline inhibits LPS priming of NLRP3 and reduces tumor progression through early apoptosis in cancer.
dc.description.sponsorshipUK Research & Innovation (UKRI) - Medical Research Council UK (MRC) - MR/P010334/1
dc.description.sponsorshipRussian President's grant - MK-3571.2021.1.4
dc.identifier.doi10.3390/ph14090852
dc.identifier.eissn1424-8247
dc.identifier.issue9
dc.identifier.urihttps://doi.org/10.3390/ph14090852
dc.identifier.urihttps://www.mdpi.com/1424-8247/14/9/852
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8466018/
dc.identifier.urihttps://hdl.handle.net/11452/42221
dc.identifier.volume14
dc.identifier.wos000701824500001
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherMdpi
dc.relation.journalPharmaceuticals
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectBenign prostatic hyperplasia
dc.subjectMediated apoptosis
dc.subjectProliferation
dc.subjectInflammasomes
dc.subjectInhibition
dc.subjectMechanisms
dc.subjectInduction
dc.subjectTherapy
dc.subjectAlpha
dc.subjectDoxycycline
dc.subjectNod-like receptor protein 3 (NLRP3)
dc.subjectInflammasome
dc.subjectApoptosis
dc.subjectCancer
dc.subjectPharmacology & pharmacy
dc.titleDoxycycline attenuates cancer cell growth by suppressing NLRP3-mediated inflammation
dc.typeArticle
dspace.entity.typePublication
relation.isAuthorOfPublicatione171a866-0a2e-4df4-9f4b-d9058971c979
relation.isAuthorOfPublication.latestForDiscoverye171a866-0a2e-4df4-9f4b-d9058971c979

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