CAR T Cells Engineered to Secrete IFNκ Induce Tumor Ferroptosis via an IFNAR/STAT1/ACSL4 Axis DOI Creative Commons
Yaoxin Gao, Shasha Liu,

Yifan Huang

et al.

Cancer Immunology Research, Journal Year: 2024, Volume and Issue: 12(12), P. 1691 - 1702

Published: Aug. 26, 2024

Abstract Ferroptosis is an iron-dependent form of cell death that influences cancer immunity. Therapeutic modulation ferroptosis considered a potential strategy to enhance the efficacy other therapies, including immunotherapies such as chimeric antigen receptor (CAR) T-cell therapy. In this study, we demonstrated IFNκ influenced induction ferroptosis. could sensitivity tumor cells induced by small molecule compound erastin and polyunsaturated fatty acid arachidonic acid. Mechanistically, in combination with immunogenic via IFNAR/STAT1/ACSL4 axis. Moreover, CAR T engineered express showed increased antitumor efficiency against H460 (antigen positive) H322 (antigen-negative) both vitro vivo. We conclude cytokine be harnessed function inducing

Language: Английский

Pharmacological inhibition of cGAS ameliorates postoperative cognitive dysfunction by suppressing caspase-3/GSDME-dependent pyroptosis DOI

Xueshan Bu,

Ping Gong, Lei Zhang

et al.

Neurochemistry International, Journal Year: 2024, Volume and Issue: 178, P. 105788 - 105788

Published: June 5, 2024

Language: Английский

Citations

8

Orexin-A alleviates ferroptosis by activating the Nrf2/HO-1 signaling pathway in traumatic brain injury DOI Creative Commons

Junwei Kang,

Bingkai Ren,

Lianghua Huang

et al.

Aging, Journal Year: 2024, Volume and Issue: 16(4), P. 3404 - 3419

Published: Feb. 12, 2024

Background: Traumatic Brain Injury (TBI) has high disability and mortality rate. Oxidative stress ferroptosis are important pathophysiological characteristics after TBI. Orexin-A (OXA) can alleviate neuronal damage in diverse neurological disorders. Nevertheless, the role mechanism of OXA TBI stay unknown. Objectives: The research investigated protection influence on its potential mechanisms. Methods: Male Sprague-Dawley rats were randomly grouped into: sham, TBI, + normal saline (NS) TBI+OXA groups. model was constructed rat via modified Feeney’s approach, treatment administered following construction model. Results: Relative to TBI+NS group, group displayed greatly recovered tissue deficits. Additionally, eased oxidative as well cerebral cortex Furthermore, increased Nrf2 expression regulating factors HO-1 NQO1 rats. Conclusions: Our found may restrain Nrf2/HO-1 signaling pathway activation, thereby reducing brain injury

Language: Английский

Citations

7

Microglial gp91phox-mediated neuroinflammation and ferroptosis contributes to learning and memory deficits in rotenone-treated mice DOI
Lü Tian, Peiyan Tang, Jianing Liu

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 220, P. 56 - 66

Published: April 30, 2024

Language: Английский

Citations

7

Hypoxic-Ischemic Encephalopathy: Pathogenesis and Promising Therapies DOI
Mingming Yang, Kexin Wang, Boya Liu

et al.

Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown

Published: July 29, 2024

Language: Английский

Citations

7

CAR T Cells Engineered to Secrete IFNκ Induce Tumor Ferroptosis via an IFNAR/STAT1/ACSL4 Axis DOI Creative Commons
Yaoxin Gao, Shasha Liu,

Yifan Huang

et al.

Cancer Immunology Research, Journal Year: 2024, Volume and Issue: 12(12), P. 1691 - 1702

Published: Aug. 26, 2024

Abstract Ferroptosis is an iron-dependent form of cell death that influences cancer immunity. Therapeutic modulation ferroptosis considered a potential strategy to enhance the efficacy other therapies, including immunotherapies such as chimeric antigen receptor (CAR) T-cell therapy. In this study, we demonstrated IFNκ influenced induction ferroptosis. could sensitivity tumor cells induced by small molecule compound erastin and polyunsaturated fatty acid arachidonic acid. Mechanistically, in combination with immunogenic via IFNAR/STAT1/ACSL4 axis. Moreover, CAR T engineered express showed increased antitumor efficiency against H460 (antigen positive) H322 (antigen-negative) both vitro vivo. We conclude cytokine be harnessed function inducing

Language: Английский

Citations

7