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Tytuł pozycji:

Ferroptosis resistance determines high susceptibility of murine A/J strain to iron-induced renal carcinogenesis.

Tytuł:
Ferroptosis resistance determines high susceptibility of murine A/J strain to iron-induced renal carcinogenesis.
Autorzy:
Cheng Z; Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Akatsuka S; Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Li GH; Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Mori K; Graduate School of Public Health, Shizuoka Graduate University of Public Health, Shizuoka, Japan.; Department of Molecular and Clinical Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan.; Department of Nephrology and Kidney Research, Shizuoka General Hospital, Shizuoka, Japan.
Takahashi T; Aichi Cancer Center Research Institute, Nagoya, Japan.
Toyokuni S; Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.; Center for Low-temperature Plasma Sciences, Nagoya University, Nagoya, Japan.
Źródło:
Cancer science [Cancer Sci] 2022 Jan; Vol. 113 (1), pp. 65-78. Date of Electronic Publication: 2021 Nov 23.
Typ publikacji:
Comparative Study; Journal Article
Język:
English
Imprint Name(s):
Publication: 2005- : Oxford : Wiley Publishing on behalf of the Japanese Cancer Association
Original Publication: Tokyo : Japanese Cancer Association, c2003-
MeSH Terms:
Gene Regulatory Networks*
Sequence Deletion*
Carcinoma, Renal Cell/*pathology
Ferric Compounds/*adverse effects
Kidney Neoplasms/*pathology
Nitrilotriacetic Acid/*analogs & derivatives
Animals ; Carcinoma, Renal Cell/chemically induced ; Carcinoma, Renal Cell/genetics ; Cationic Amino Acid Transporter 1/genetics ; Cyclin-Dependent Kinase Inhibitor p15/genetics ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Ferritins/genetics ; Ferroptosis ; Gene Expression Regulation, Neoplastic ; Homozygote ; Injections, Intraperitoneal ; Kidney Neoplasms/chemically induced ; Kidney Neoplasms/genetics ; Lipid Peroxidation ; Lipocalin-2/genetics ; Male ; Mice ; Neoplasms, Experimental ; Nitrilotriacetic Acid/adverse effects ; Oxidative Stress ; Receptors, Transferrin/genetics ; Species Specificity ; Up-Regulation
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Grant Information:
JPMJCR19H4 JST CREST; JP19H05462 JSPS; JP20H05502 JSPS; Princess Takamatsu Cancer Research
Contributed Indexing:
Keywords: animal models; ferroptosis; iron; lipocalins; renal cell carcinoma
Substance Nomenclature:
0 (Cationic Amino Acid Transporter 1)
0 (Cdkn2a protein, mouse)
0 (Cdkn2b protein, mouse)
0 (Cyclin-Dependent Kinase Inhibitor p15)
0 (Cyclin-Dependent Kinase Inhibitor p16)
0 (Ferric Compounds)
0 (Lipocalin-2)
0 (Receptors, Transferrin)
0 (Slc7a1 protein, mouse)
126469-30-5 (Lcn2 protein, mouse)
9007-73-2 (Ferritins)
KA90006V9D (Nitrilotriacetic Acid)
Z3U5ED15B9 (ferric nitrilotriacetate)
Entry Date(s):
Date Created: 20211026 Date Completed: 20220112 Latest Revision: 20220115
Update Code:
20240105
PubMed Central ID:
PMC8748236
DOI:
10.1111/cas.15175
PMID:
34699654
Czasopismo naukowe
Cancer susceptibility is a critical factor in the understanding of carcinogenesis. Intraperitoneal (i.p.) injection of an iron chelate, ferric nitrilotriacetate (Fe-NTA), produces hydroxyl radicals via Fenton reaction to induce ferroptosis in renal proximal tubules. Rats or mice subjected to repeated i.p. injections of Fe-NTA develop renal cell carcinoma (RCC). To elucidate the molecular mechanisms that cause susceptibility to renal carcinogenesis, we first established an inter-strain difference in the susceptibility to Fe-NTA-induced renal carcinogenesis in mice. Based on a previous observation of a low incidence of RCC with this model in C57BL/6J strain mice, we investigated A/J strain mice here, which demonstrated significantly higher susceptibility to Fe-NTA-induced renal carcinogenesis. Homozygous deletion of the Cdkn2a/2b tumor suppressor locus was detected for the first time in A/J strain mice. Focusing on ferroptosis and iron metabolism, we explored the mechanisms involved that lead to the difference in RCC development. We compared the protective responses in the kidney of A/J and C57BL/6J strains after Fe-NTA treatment. After 3-week Fe-NTA treatment, A/J mice maintained higher levels of expression of glutathione peroxidase 4 and xCT (SLC7A11), leading to a lower level of lipid peroxidation. Simultaneously, A/J mice had decreased expression of transferrin receptor and increased expression of ferritin to greater degrees than C57BL/6 mice. After a single Fe-NTA injection, higher levels of oxidative cell damage and cytosolic catalytic Fe(II) were observed in C57BL/6J mice, accompanied by a greater increase in lipocalin-2. Lipocalin-2 deficiency significantly decreased oxidative renal damage. Our results suggest that a genetic trait favoring ferroptosis resistance contributes to high susceptibility to Fe-NTA-induced RCC in A/J strain.
(© 2021 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.)

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