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TFRC upregulation promotes ferroptosis in CVB3 infection via nucleus recruitment of Sp1
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TFRC upregulation promotes ferroptosis in CVB3 infection via nucleus recruitment of Sp1
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TFRC upregulation promotes ferroptosis in CVB3 infection via nucleus recruitment of Sp1
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Journal Article
TFRC upregulation promotes ferroptosis in CVB3 infection via nucleus recruitment of Sp1
2022
Overview
CVB3 is a single positive-strand enterovirus, and a common pathogen in myocarditis etiology. Although a number of antiviral candidates are under development, specific targeted therapy is not available for CVB3. Ferroptosis is a new type of regulatory cell death discovered in recent years. In this study, our team provided the first evidence that ferroptosis existed in CVB3 infection in vivo and in vitro by iron overload, and massive accumulation of lipid peroxides. Mechanistically, we construct a classical model of HeLa cells following a time-course infection (6, 12, 24, 36, 48 h) with CVB3 (MOI = 10). We demonstrated that the
TFRC
gene plays an important role in promoting ferroptosis in CVB3 infection and downregulation of
TFRC
attenuated the ferroptosis. Interestingly, we observed that
TFRC
was nuclear translocation induced by the CVB3, which was predominantly localized in the cell membrane, but redistributed to the nucleus during CVB3 infection. Moreover, we found that the transcription factor
Sp1
was an essential factor that could bind to the
TFRC
promoter and upregulate the
TFRC
transcription. Collectively, these results suggest that the Sp1/TFRC/Fe axis may provide a new target for the development of therapies against CVB3 infection.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ 13/31
/ 13/56
/ 13/89
/ 14/1
/ 14/34
/ 38/1
/ 42/89
/ 64/60
/ 692/699
/ 82/29
/ Biomedical and Life Sciences
/ Coxsackievirus Infections - genetics
/ Coxsackievirus Infections - metabolism
/ Etiology
/ Humans
/ Receptors, Transferrin - genetics
/ Receptors, Transferrin - metabolism
/ Sp1 Transcription Factor - genetics
