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Tytuł pozycji:

Rab GTPase Mediating Regulation of NALP3 in Colorectal Cancer.

Tytuł:
Rab GTPase Mediating Regulation of NALP3 in Colorectal Cancer.
Autorzy:
Tezcan G; Institution of Fundamental Medicine and Biology, Kazan Federal University, 420008 Kazan, Russia.; Faculty of Dentistry, Department of Fundamental Sciences, Bursa Uludag University, Bursa 16240, Turkey.
Garanina EE; Institution of Fundamental Medicine and Biology, Kazan Federal University, 420008 Kazan, Russia.
Zhuravleva MN; Institution of Fundamental Medicine and Biology, Kazan Federal University, 420008 Kazan, Russia.
Hamza S; Institution of Fundamental Medicine and Biology, Kazan Federal University, 420008 Kazan, Russia.
Rizvanov AA; Institution of Fundamental Medicine and Biology, Kazan Federal University, 420008 Kazan, Russia.
Khaiboullina SF; Institution of Fundamental Medicine and Biology, Kazan Federal University, 420008 Kazan, Russia.; Department of Microbiology and Immunology, University of Nevada, Reno, NV 89557, USA.
Źródło:
Molecules (Basel, Switzerland) [Molecules] 2020 Oct 20; Vol. 25 (20). Date of Electronic Publication: 2020 Oct 20.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, c1995-
MeSH Terms:
Colorectal Neoplasms/*genetics
NLR Family, Pyrin Domain-Containing 3 Protein/*genetics
rab GTP-Binding Proteins/*genetics
rab5 GTP-Binding Proteins/*genetics
Caspase 1/genetics ; Colorectal Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; HCT116 Cells ; Humans ; Inflammasomes/genetics ; Inflammation/genetics ; Inflammation/pathology ; Interleukin-1beta/genetics ; Signal Transduction/genetics ; rab7 GTP-Binding Proteins
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Grant Information:
18-34-01000 Russian Foundation for Basic Research
Contributed Indexing:
Keywords: NALP3; Rab GTPase; colorectal cancer; inflammasome signalling; vesicle trafficking pathway
Substance Nomenclature:
0 (IL1B protein, human)
0 (Inflammasomes)
0 (Interleukin-1beta)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
0 (NLRP3 protein, human)
0 (rab7 GTP-Binding Proteins)
0 (rab7 GTP-binding proteins, human)
EC 3.4.22.36 (Caspase 1)
EC 3.6.1.- (RAB39A protein, human)
EC 3.6.1.- (RAB5C protein, human)
EC 3.6.1.- (rab11 protein)
EC 3.6.5.2 (rab GTP-Binding Proteins)
EC 3.6.5.2 (rab5 GTP-Binding Proteins)
Entry Date(s):
Date Created: 20201023 Date Completed: 20210325 Latest Revision: 20211204
Update Code:
20240105
PubMed Central ID:
PMC7587934
DOI:
10.3390/molecules25204834
PMID:
33092247
Czasopismo naukowe
The NALP3 inflammasome signaling contributes to inflammation within tumor tissues. This inflammation may be promoted by the vesicle trafficking of inflammasome components and cytokines. Rab5, Rab7 and Rab11 regulate vesicle trafficking. However, the role of these proteins in the regulation of inflammasomes remains largely unknown. To elucidate the role of these Rab proteins in inflammasome regulation, HCT-116, a colorectal cancer (CRC) cell line expressing pDsRed-Rab5 wild type (WT), pDsRed-Rab5 dominant-negative (DN), pDsRed-Rab7 WT, pDsRed-Rab7 DN, pDsRed-Rab11 WT and pDsRed-Rab11 DN were treated with lipopolysaccharide (LPS)/nigericin. Inflammasome activation was analyzed by measuring the mRNA expression of NLRP3 , Pro-CASP1 , RAB39A and Pro-IL-1β , conducting immunofluorescence imaging and western blotting of caspase-1 and analysing the secretion levels of IL-1β using enzyme-linked immunosorbent assay (ELISA). The effects of Rabs on cytokine release were evaluated using MILLIPLEX MAP Human Cytokine/Chemokine Magnetic Bead Panel-Premixed 41 Plex. The findings showed that LPS/nigericin-treated cells expressing Rab5-WT indicated increased NALP3 expression and secretion of the IL-1β as compared to Rab5-DN cells. Caspase-1 was localized in the nucleus and cytosol of Rab5-WT cells but was localized in the cytosol in Rab5-DN cells. There were no any effects of Rab7 and Rab11 expression on the regulation of inflammasomes. Our results suggest that Rab5 may be a potential target for the regulation of NALP3 in the treatment of the CRC inflammation.
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