A small molecule cryptotanshinone induces non-enzymatic NQO1-dependent necrosis in cancer cells through the JNK1/2/Iron/PARP/calcium pathway DOI Creative Commons
Ying Hou, Bingling Zhong, Lin Zhao

et al.

Acta Pharmaceutica Sinica B, Journal Year: 2024, Volume and Issue: 15(2), P. 991 - 1006

Published: Dec. 9, 2024

Human NAD(P)H: quinone oxidoreductase 1 (NQO1) is a flavoenzyme expressed at high levels in multiple solid tumors, making it an attractive target for anticancer drugs. Bioactivatable drugs targeting NQO1, such as β-lapachone (β-lap), are currently clinical trials the treatment of cancer. β-Lap selectively kills NQO1-positive (NQO1+) cancer cells by inducing reactive oxygen species (ROS) via catalytic activation NQO1. In this study, we demonstrated that cryptotanshinone (CTS), naturally occurring compound, induces NQO1-dependent necrosis without affecting NQO1 activity. CTS NQO1+ necrosis. Interestingly, directly binds to but does not activate its addition, enables JNK1/2 and PARP, accumulation iron Ca2+, depletion ATP NAD+. Furthermore, suppressed tumor growth xenograft models, which was reversed inhibitor shRNA. conclusion, JNK1/2/iron/PARP/NAD+/Ca2+ signaling pathway. This study demonstrates non-enzymatic function cell death provides new avenues design development NQO1-targeted

Language: Английский

Sonodynamic Activated Nanoparticles with Glut1 Inhibitor and Cystine-containing Polymer Stimulate Disulfidptosis for Improved Immunotherapy in Bladder Cancer DOI Creative Commons
Ke Wang, Li Li,

Ganghao Liang

et al.

Biomaterials, Journal Year: 2025, Volume and Issue: 319, P. 123178 - 123178

Published: Feb. 8, 2025

Language: Английский

Citations

2
Unusual chaetoglobosins and a new type of ferroptosis inducer from an endophytic fungus Chaetomium sp. UJN-EF006 DOI
Yinyin Wang,

Yu-Song Wang,

Jun‐Jiang Li

et al.

Bioorganic Chemistry, Journal Year: 2025, Volume and Issue: 158, P. 108342 - 108342

Published: March 6, 2025

Language: Английский

Citations

0
Targeting regulated cell death: Apoptosis, necroptosis, pyroptosis, ferroptosis, and cuproptosis in anticancer immunity DOI
Ziyu Guo,

Yihuang Liu,

Danyao Chen

et al.

Journal of Translational Internal Medicine, Journal Year: 2025, Volume and Issue: 13(1), P. 10 - 32

Published: Feb. 1, 2025

In the evolving landscape of cancer treatment, strategic manipulation regulated cell death (RCD) pathways has emerged as a crucial component effective anti-tumor immunity. Evidence suggests that tumor cells undergoing RCD can modify immunogenicity microenvironment (TME), potentially enhancing its ability to suppress progression and metastasis. this review, we first explore mechanisms apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, along with crosstalk between these modalities. We then discuss how processes activate antigen-presenting cells, facilitate cross-priming CD8+ T trigger immune responses, highlighting complex effects novel forms on TME biology. Furthermore, summarize potential drugs nanoparticles induce or inhibit emerging their therapeutic roles in treatment. Finally, put forward existing challenges future prospects for targeting anti-cancer Overall, review enhances our understanding molecular biological impacts RCD-based therapies, providing new perspectives strategies

Language: Английский

Citations

0
Ultrasound-responsive nanobubble-mediated sonodynamic therapy sensitizes disulfidptosis in the treatment of liver hepatocellular carcinoma DOI Creative Commons
Yichi Chen, Xin Lin, Jiayue Qiu

et al.

Ultrasonics Sonochemistry, Journal Year: 2025, Volume and Issue: 118, P. 107368 - 107368

Published: April 23, 2025

Disulfidptosis, a newly identified regulated cell death, is linked to tumor progression, particularly in cancers with elevated SLC7A11 expression. This study investigates expression liver hepatocellular carcinoma (LIHC) and evaluates the therapeutic potential of ICG@C3F8-KL nanobubbles (NBs) combined sonodynamic therapy (SDT) for inducing disulfidptosis. Bioinformatics analysis TCGA datasets revealed upregulation LIHC tissues. The synthesized NBs exhibited mean diameter 156.46 nm stable properties, high encapsulation efficiencies 51.32 % ± 0.7 KL 80.15 0.21 ICG. In vitro, NBs, under ultrasound, generated reactive oxygen species (ROS), enhancing cytotoxicity HepG2 cells an IC50 lower than alone. These also inhibited migration colony formation, suggesting disulfidptosis induction via altered glucose uptake NADP+/NADPH ratio, as well F-actin contraction. vivo, accumulated tissues suppressed growth without significant toxicity. Unsupervised clustering disulfidptosis-related genes cohort subtypes distinct prognoses, predictive model based on five key was developed. conclusion, effectively induce disulfidptosis, offering promising strategy treatment, personalized informed by disulfide-associated gene signatures.

Language: Английский

Citations

0
The molecular mechanisms, roles, and potential applications of PANoptosis in cancer treatment DOI Creative Commons
Wenyuan Ma, Qiang Wang,

Lanfang Guo

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: April 29, 2025

PANoptosis, a newly identified form of programmed cell death regulated by the panoptosome complex, exhibits key characteristics apoptosis, pyroptosis and necroptosis. It exerts substantial influence on initiation progression spectrum diseases, particularly in cancer, where its impact is increasingly being recognized. PANoptosis closely related to tumorigenesis, carcinogenesis, metastasis, chemotherapy resistance, as well prediction therapeutic responses prognosis cancer patients. In this review, we first review discovery systematically analyze composition panoptosome. Subsequently, examine role various types encompassing function within tumor microenvironment, drug predictive prognosis. Ultimately, delve into strategies for targeting therapy, including molecules pathway, such ZBP1, RIPK1, RIPK3, Caspases other novel like nanoinducers viral vectors. This aims provide references assistance research application treatment.

Language: Английский

Citations

0
Biomimic Nanodrugs Overcome Tumor Immunosuppressive Microenvironment to Enhance Cuproptosis/Chemodynamic‐Induced Cancer Immunotherapy DOI Creative Commons
Hangyi Wu, Xiaoyu Lu, Yuhan Hu

et al.

Advanced Science, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 12, 2024

Elesclomol (ES) as an efficient Cu ionophore can specifically transport into mitochondria and disrupt intracellular homeostasis. Extra induces cuproptosis chemodynamic therapy (CDT), which further cascades immunogenic cell death (ICD) activates antitumor immune responses. However, the tumor immunosuppressive microenvironment (TIM) attenuates efficiency of response. Herein, a biomimic nanodrug (ECNM) is fabricated, ES,

Language: Английский

Citations

1
Targeting regulated cell death (RCD) with naturally derived sesquiterpene lactones in cancer therapy DOI Creative Commons
Cong Xu, Shaodi Wen, Xiaoyue Du

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: unknown, P. 107553 - 107553

Published: Dec. 1, 2024

Language: Английский

Citations

1
Excavating regulated cell death signatures to predict prognosis, tumor microenvironment and therapeutic response in HR+/HER2- breast cancer DOI Creative Commons
Shuangshuang Mao, Yuanyuan Zhao,

Huihua Xiong

et al.

Translational Oncology, Journal Year: 2024, Volume and Issue: 50, P. 102117 - 102117

Published: Sept. 6, 2024

Language: Английский

Citations

0
Discovery of phenazine derivatives as a new class of non-classical ferroptosis inhibitors and efficacy evaluation on a mouse model of liver injury DOI
Yunjie Wu, Yang Lu, Jing You

et al.

European Journal of Medicinal Chemistry, Journal Year: 2024, Volume and Issue: 282, P. 117042 - 117042

Published: Nov. 12, 2024

Language: Английский

Citations

0
A small molecule cryptotanshinone induces non-enzymatic NQO1-dependent necrosis in cancer cells through the JNK1/2/Iron/PARP/calcium pathway DOI Creative Commons
Ying Hou, Bingling Zhong, Lin Zhao

et al.

Acta Pharmaceutica Sinica B, Journal Year: 2024, Volume and Issue: 15(2), P. 991 - 1006

Published: Dec. 9, 2024

Human NAD(P)H: quinone oxidoreductase 1 (NQO1) is a flavoenzyme expressed at high levels in multiple solid tumors, making it an attractive target for anticancer drugs. Bioactivatable drugs targeting NQO1, such as β-lapachone (β-lap), are currently clinical trials the treatment of cancer. β-Lap selectively kills NQO1-positive (NQO1+) cancer cells by inducing reactive oxygen species (ROS) via catalytic activation NQO1. In this study, we demonstrated that cryptotanshinone (CTS), naturally occurring compound, induces NQO1-dependent necrosis without affecting NQO1 activity. CTS NQO1+ necrosis. Interestingly, directly binds to but does not activate its addition, enables JNK1/2 and PARP, accumulation iron Ca2+, depletion ATP NAD+. Furthermore, suppressed tumor growth xenograft models, which was reversed inhibitor shRNA. conclusion, JNK1/2/iron/PARP/NAD+/Ca2+ signaling pathway. This study demonstrates non-enzymatic function cell death provides new avenues design development NQO1-targeted

Language: Английский

Citations

0