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  1. Article: Implications of NLRP3 Suppression Using Glibenclamide and miR-223 against Colorectal Cancer.

    Hamza, Shaimaa / Garanina, Ekaterina E / Shkair, Layaly / Alsaadi, Mohammad / Khaiboullina, Svetlana F / Tezcan, Gulcin

    Pharmaceuticals (Basel, Switzerland)

    2024  Volume 17, Issue 3

    Abstract: The NLR family pyrin domain containing 3 (NLRP3) promotes the growth of colorectal cancer (CRC). However, the therapeutic effect of NLRP3 inhibition on CRC cell progression is controversial. This study comparatively investigated the therapeutic effect of ...

    Abstract The NLR family pyrin domain containing 3 (NLRP3) promotes the growth of colorectal cancer (CRC). However, the therapeutic effect of NLRP3 inhibition on CRC cell progression is controversial. This study comparatively investigated the therapeutic effect of a pharmacological NLRP3 inhibitor, glibenclamide (gli), and the post-translational suppression of NLRP3 by miR-223 on CRC cell progression in HCT-116 and HCT-15 cells. LPS and ATP were used to activate Gli-treated and LSB-hsa-miR-223-3p (WT
    Language English
    Publishing date 2024-02-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph17030299
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Blocking the Hormone Receptors Modulates NLRP3 in LPS-Primed Breast Cancer Cells.

    Hamza, Shaimaa / Garanina, Ekaterina E / Alsaadi, Mohammad / Khaiboullina, Svetlana F / Tezcan, Gulcin

    International journal of molecular sciences

    2023  Volume 24, Issue 5

    Abstract: NOD-like receptor protein 3 (NLRP3) may contribute to the growth and propagation of breast cancer (BC). The effect of estrogen receptor-α (ER-α), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) on NLRP3 activation in BC ... ...

    Abstract NOD-like receptor protein 3 (NLRP3) may contribute to the growth and propagation of breast cancer (BC). The effect of estrogen receptor-α (ER-α), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) on NLRP3 activation in BC remains unknown. Additionally, our knowledge of the effect of blocking these receptors on NLRP3 expression is limited. We used GEPIA, UALCAN, and the Human Protein Atlas for transcriptomic profiling of NLRP3 in BC. Lipopolysaccharide (LPS) and adenosine 5'-triphosphate (ATP) were used to activate NLRP3 in luminal A MCF-7 and in TNBC MDA-MB-231 and HCC1806 cells. Tamoxifen (Tx), mifepristone (mife), and trastuzumab (Tmab) were used to block ER-α, PR, and HER2, respectively, on inflammasome activation in LPS-primed MCF7 cells. The transcript level of
    MeSH term(s) Female ; Humans ; Adenosine Triphosphate/metabolism ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Interleukin-8/metabolism ; Lipopolysaccharides ; MCF-7 Cells ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Tamoxifen/pharmacology ; Estrogen Receptor alpha/antagonists & inhibitors ; Estrogen Receptor alpha/metabolism ; Receptors, Progesterone/antagonists & inhibitors ; Receptor, ErbB-2/antagonists & inhibitors ; Estrogen Antagonists/pharmacology
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; Interleukin-8 ; Lipopolysaccharides ; NLR Family, Pyrin Domain-Containing 3 Protein ; Tamoxifen (094ZI81Y45) ; Estrogen Receptor alpha ; Receptors, Progesterone ; Receptor, ErbB-2 (EC 2.7.10.1) ; Estrogen Antagonists
    Language English
    Publishing date 2023-03-02
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24054846
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Doxycycline Attenuates Cancer Cell Growth by Suppressing NLRP3-Mediated Inflammation.

    Alsaadi, Mohammad / Tezcan, Gulcin / Garanina, Ekaterina E / Hamza, Shaimaa / McIntyre, Alan / Rizvanov, Albert A / Khaiboullina, Svetlana F

    Pharmaceuticals (Basel, Switzerland)

    2021  Volume 14, Issue 9

    Abstract: NLR 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. ...

    Abstract NLR 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-IL1β using RT-qPCR. Additionally, NLPR3 protein expression and IL-1β 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 (
    Language English
    Publishing date 2021-08-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph14090852
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Azithromycin and Ceftriaxone Differentially Activate NLRP3 in LPS Primed Cancer Cells.

    Tezcan, Gulcin / Alsaadi, Mohammad / Hamza, Shaimaa / Garanina, Ekaterina E / Martynova, Ekaterina V / Ziganshina, Gulshat R / Farukshina, Elina R / Rizvanov, Albert A / Khaiboullina, Svetlana F

    International journal of molecular sciences

    2022  Volume 23, Issue 16

    Abstract: Background: Cancer patients are prescribed antibiotics, such as macrolides and lactamides, for infection treatment. However, the effect of these antibiotics on NLRP3 activation remains largely unknown.: Method: Lung cancer (A549) and prostate cancer ( ...

    Abstract Background: Cancer patients are prescribed antibiotics, such as macrolides and lactamides, for infection treatment. However, the effect of these antibiotics on NLRP3 activation remains largely unknown.
    Method: Lung cancer (A549) and prostate cancer (PC3) cell lines were primed with lipopolysaccharide (LPS) to activate NLRP3 transcription. Cells were then treated with azithromycin (Az) or ceftriaxone (Cf). NLRP3 activation was analyzed by qPCR, Western blot, and ELISA. Cell growth and viability were assessed by real-time cell analysis and Annexin V expression. Levels of 41 cytokines were also analyzed using a multiplex assay.
    Results: LPS-Az activated transcription of
    Discussion: Our data suggest that Cf could suppress LPS induced NLRP3, which should be considered when selecting antibiotics for cancer treatment. In contrast, the effect of Az on LPS primed NLRP3 and the inflammatory cytokines production appears to depend on the cancer cell origin. Therefore, these data indicate that considerations are required when selecting Az for the treatment of cancer patients.
    MeSH term(s) Azithromycin/pharmacology ; Ceftriaxone/pharmacology ; Cell Line, Tumor ; Cytokines/metabolism ; Humans ; Inflammasomes/metabolism ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Lipopolysaccharides/pharmacology ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Neoplasms
    Chemical Substances Cytokines ; Inflammasomes ; Interleukin-1beta ; Lipopolysaccharides ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Ceftriaxone (75J73V1629) ; Azithromycin (83905-01-5)
    Language English
    Publishing date 2022-08-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23169484
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Therapeutic Potential of Pharmacological Targeting NLRP3 Inflammasome Complex in Cancer.

    Tezcan, Gulcin / Garanina, Ekaterina E / Alsaadi, Mohammad / Gilazieva, Zarema E / Martinova, Ekaterina V / Markelova, Maria I / Arkhipova, Svetlana S / Hamza, Shaimaa / McIntyre, Alan / Rizvanov, Albert A / Khaiboullina, Svetlana F

    Frontiers in immunology

    2021  Volume 11, Page(s) 607881

    Abstract: Introduction: Dysregulation of NLRP3 inflammasome complex formation can promote chronic inflammation by increased release of IL-1β. However, the effect of NLRP3 complex formation on tumor progression remains controversial. Therefore, we sought to ... ...

    Abstract Introduction: Dysregulation of NLRP3 inflammasome complex formation can promote chronic inflammation by increased release of IL-1β. However, the effect of NLRP3 complex formation on tumor progression remains controversial. Therefore, we sought to determine the effect of NLRP3 modulation on the growth of the different types of cancer cells, derived from lung, breast, and prostate cancers as well as neuroblastoma and glioblastoma
    Method: The effect of Caspase 1 inhibitor (VX765) and combination of LPS/Nigericin on NLRP3 inflammasome activity was analyzed in A549 (lung cancer), MCF-7 (breast cancer), PC3 (prostate cancer), SH-SY5Y (neuroblastoma), and U138MG (glioblastoma) cells. Human fibroblasts were used as control cells. The effect of VX765 and LPS/Nigericin on NLRP3 expression was analyzed using western blot, while IL-1β and IL-18 secretion was detected by ELISA. Tumor cell viability and progression were determined using Annexin V, cell proliferation assay, LDH assay, sphere formation assay, transmission electron microscopy, and a multiplex cytokine assay. Also, angiogenesis was investigated by a tube formation assay. VEGF and MMPs secretion were detected by ELISA and a multiplex assay, respectively. Statistical analysis was done using one-way ANOVA with Tukey's analyses and Kruskal-Wallis one-way analysis of variance.
    Results: LPS/Nigericin increased NRLP3 protein expression as well as IL-1β and IL-18 secretion in PC3 and U138MG cells compared to A549, MCF7, SH-SY5Y cells, and fibroblasts. In contrast, MIF expression was commonly found upregulated in A549, PC3, SH-SY5Y, and U138MG cells and fibroblasts after Nigericin treatment. Nigericin and a combination of LPS/Nigericin decreased the cell viability and proliferation. Also, LPS/Nigericin significantly increased tumorsphere size in PC3 and U138MG cells. In contrast, the sphere size was reduced in MCF7 and SH-SY5Y cells treated with LPS/Nigericin, while no effect was detected in A549 cells. VX765 increased secretion of CCL24 in A549, MCF7, PC3, and fibroblasts as well as CCL11 and CCL26 in SH-SY5Y cells. Also, VX765 significantly increased the production of VEGF and MMPs and stimulated angiogenesis in all tumor cell lines.
    Discussion: Our data suggest that NLRP3 activation using Nigericin could be a novel therapeutic approach to control the growth of tumors producing a low level of IL-1β and IL-18.
    MeSH term(s) A549 Cells ; Antineoplastic Agents/pharmacology ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cytokines/metabolism ; Dipeptides/pharmacology ; Humans ; Inflammasomes/agonists ; Inflammasomes/antagonists & inhibitors ; Inflammasomes/metabolism ; Inflammation Mediators/metabolism ; MCF-7 Cells ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Molecular Targeted Therapy ; NLR Family, Pyrin Domain-Containing 3 Protein/agonists ; NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Neovascularization, Pathologic ; Nigericin/pharmacology ; PC-3 Cells ; Signal Transduction ; para-Aminobenzoates/pharmacology
    Chemical Substances Antineoplastic Agents ; Cytokines ; Dipeptides ; Inflammasomes ; Inflammation Mediators ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; para-Aminobenzoates ; belnacasan (00OLE78529) ; Nigericin (RRU6GY95IS)
    Language English
    Publishing date 2021-02-03
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.607881
    Database MEDical Literature Analysis and Retrieval System OnLINE

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