Advances in non-apoptotic regulated cell death: implications for malignant tumor treatment DOI Creative Commons
Yizheng Zhang,

Shiqi Yi,

Mingyuan Luan

и другие.

Frontiers in Oncology, Год журнала: 2025, Номер 15

Опубликована: Янв. 30, 2025

Cell death mechanisms are broadly classified into accidental cell (ACD) and regulated (RCD). ACD such as necrosis, is an uncontrolled, process, while RCD tightly by specific signaling pathways molecular mechanisms. Tumor cells characterized their ability to evade sustain uncontrolled proliferation. The failure of programmed a key contributor tumor initiation, progression, resistance cancer therapies. Traditionally, research has focused primarily on apoptosis the dominant form in cancer. However, emerging evidence highlights importance other non-apoptotic forms RCD, pyroptosis, ferroptosis, necroptosis, parthanatos, tumorigenesis treatment response. These gaining attention for potential roles overcoming therapy resistance. In this review, we will discuss recent advances study malignant tumors explore therapeutic implications, offering insights new targets strategies.

Язык: Английский

CHMP4C promotes pancreatic cancer progression by inhibiting necroptosis via the RIPK1/RIPK3/MLKL pathway DOI Creative Commons

Longchen Yu,

Qining Guo,

Yaping Li

и другие.

Journal of Advanced Research, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

2
A RIPK1-specific PROTAC degrader achieves potent antitumor activity by enhancing immunogenic cell death DOI Creative Commons
Jonathan Mannion, Valentina Gifford, Benjamin R. Bellenie

и другие.

Immunity, Год журнала: 2024, Номер 57(7), С. 1514 - 1532.e15

Опубликована: Май 23, 2024

Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) functions as a critical stress sentinel that coordinates cell survival, inflammation, and immunogenic death (ICD). Although the catalytic function of RIPK1 is required to trigger death, its non-catalytic scaffold mediates strong pro-survival signaling. Accordingly, cancer cells can hijack block necroptosis evade immune detection. We generated small-molecule proteolysis-targeting chimera (PROTAC) selectively degraded human murine RIPK1. PROTAC-mediated depletion deregulated TNFR1 TLR3/4 signaling hubs, accentuating output NF-κB, MAPK, IFN Additionally, degradation simultaneously promoted RIPK3 activation induction. further demonstrated enhanced immunostimulatory effects radio- immunotherapy by sensitizing treatment-induced TNF interferons. This ICD, antitumor immunity, durable treatment responses. Consequently, targeting PROTACs emerges promising approach overcome or resistance enhance anticancer therapies.

Язык: Английский

Процитировано

14
Cell death pathways: molecular mechanisms and therapeutic targets for cancer DOI Creative Commons
Shaohui Wang, Sa Guo, Jing Guo

и другие.

MedComm, Год журнала: 2024, Номер 5(9)

Опубликована: Сен. 1, 2024

Abstract Cell death regulation is essential for tissue homeostasis and its dysregulation often underlies cancer development. Understanding the different pathways of cell can provide novel therapeutic strategies battling cancer. This review explores several key mechanisms apoptosis, necroptosis, autophagic death, ferroptosis, pyroptosis. The research gap addressed involves a thorough analysis how these be precisely targeted therapy, considering tumor heterogeneity adaptation. It delves into genetic epigenetic factors signaling cascades like phosphatidylinositol 3‐kinase/protein kinase B/mammalian target rapamycin (PI3K/AKT/mTOR) mitogen‐activated protein kinase/extracellular signal‐regulated (MAPK/ERK) pathways, which are critical death. Additionally, interaction microenvironment with cells, particularly influence hypoxia, nutrient deprivation, immune cellular interactions, explored. Emphasizing strategies, this highlights emerging modulators inducers such as B lymphoma 2 (BCL2) homology domain 3 (BH3) mimetics, tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL), chloroquine, innovative approaches to induce ferroptosis provides insights therapy's future direction, focusing on multifaceted circumvent drug resistance. examination evolving underlines considerable clinical potential continuous necessity in‐depth exploration within scientific domain.

Язык: Английский

Процитировано

12
Recent Advances in Biomimetic Strategies for the Immunotherapy of Glioblastoma DOI

Haoyu You,

Shuo Geng,

Shangkuo Li

и другие.

Biomaterials, Год журнала: 2024, Номер 311, С. 122694 - 122694

Опубликована: Июнь 28, 2024

Язык: Английский

Процитировано

8
Dual-Enzyme-Instructed Peptide Self-Assembly to Boost Immunogenic Cell Death by Coordinating Intracellular Calcium Overload and Chemotherapy DOI
H. H. Zhang, Yuhan Hu,

Yinghao Ding

и другие.

ACS Nano, Год журнала: 2025, Номер 19(1), С. 488 - 503

Опубликована: Янв. 4, 2025

The concept of immunogenic cell death (ICD) induced by chemotherapy as a potential synergistic modality for cancer immunotherapy has been widely discussed. Unfortunately, most chemotherapeutic agents failed to dictate effective ICD responses due their defects in inducing potent signaling. Here, we report dual-enzyme-instructed peptide self-assembly platform CPMC (CPT-GFFpY-PLGVRK-Caps) that cooperatively utilizes camptothecin (CPT) and capsaicin (Caps) promote engage systemic adaptive immunity tumor rejection. Although CPT Caps respectively prevent progression inhibiting type-I DNA topoisomerase activating transient receptor cation channel subfamily V member 1 (TRPV1) intracellular calcium overload, neither alone effectively stimulates sufficient signaling meet immunotherapeutic needs. CPMC, sequentially allowing an active derivative VRK-Caps release extracellularly intracellularly, can synergize two distinct apoptosis pathways stimulated increase immunogenicity elicit T-cell-based immunity. Consequently, facilitates the generation improved tumor-specific cytotoxic T-cell sustained immunological memory, successfully suppressing both primary distant tumors. Moreover, render tumors susceptible PD-L1 blockade with antiprogrammed death-ligand (aPDL1) antibody inhibition. Combining drugs low ICD-stimulating capacity using strategy was demonstrated boost potentiate immunotherapy.

Язык: Английский

Процитировано

1
Prognostic models of immune-related cell death and stress unveil mechanisms driving macrophage phenotypic evolution in colorectal cancer DOI Creative Commons
Hao Liu, Chuhan Zhang,

Sanfei Peng

и другие.

Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)

Опубликована: Янв. 28, 2025

Tumor microenvironment (TME), particularly immune cell infiltration, programmed death (PCD) and stress, has increasingly become a focal point in colorectal cancer (CRC) treatment. Uncovering the intricate crosstalk between these factors can enhance our understanding of CRC, guide therapeutic strategies, improve patient prognosis. We constructed an immune-related stress (ICDS) prognostic model utilizing machine learning methodologies. Furthermore, we performed enrichment analyses deconvolution algorithms to elucidate complex interactions infiltration processes PCD within substantial array transcriptomic data from The Cancer Genome Atlas (TCGA) Gene Expression Omnibus base (GEO) related CRC. Single-cell sequencing biochemical experiments were used validate interaction genes tumor cells. ICDS exhibited robust predictive performance seven independent cohorts, revealing inverse correlation scores Meanwhile, index was positively correlated with clinical stage. Model analysis indicated that subgroups low heightened activation features elevated activity pathways. further revealed macrophages central drivers characteristics underlying differences model. Pseudotime cellular gene GAL3ST4 promotes transition toward M2 pro-tumor phenotype. communication experimental validation cuproptosis cells suppress expression, thereby inhibiting M2-like macrophage polarization. In summary, uncovered mechanism by which downregulate expression via inhibit polarization, providing new targets biomarkers for CRC treatment prognosis evaluation.

Язык: Английский

Процитировано

1
N7-methylguanosine modification in cancers: from mechanisms to therapeutic potential DOI Creative Commons
Qihui Wu, Xiaodan Fu,

Guoqian Liu

и другие.

Journal of Hematology & Oncology, Год журнала: 2025, Номер 18(1)

Опубликована: Янв. 29, 2025

N7-methylguanosine (m7G) is an important RNA modification involved in epigenetic regulation that commonly observed both prokaryotic and eukaryotic organisms. Their influence on the synthesis processing of messenger RNA, ribosomal transfer allows m7G modifications to affect diverse cellular, physiological, pathological processes. are pivotal human diseases, particularly cancer progression. On one hand, modification-associated modulate tumour progression malignant biological characteristics, including sustained proliferation signalling, resistance cell death, activation invasion metastasis, reprogramming energy metabolism, genome instability, immune evasion. This suggests they may be novel therapeutic targets for treatment. other aberrant expression molecules linked clinicopathological staging, lymph node unfavourable prognoses patients with cancer, indicating their potential as biomarkers. review consolidates discovery, identification, detection methodologies, functional roles modification, analysing mechanisms by which contribute development, exploring clinical applications diagnostics therapy, thereby providing innovative strategies identification targeted

Язык: Английский

Процитировано

1
MSCs Suppress Macrophage Necroptosis and Foster Liver Regeneration by Modulating SP1/SK1 Axis in Treating Acute Severe Autoimmune Hepatitis DOI Creative Commons
Ran An, Zhengyi Zhu, Yuyan Chen

и другие.

Advanced Science, Год журнала: 2025, Номер unknown

Опубликована: Фев. 3, 2025

Abstract Acute severe autoimmune hepatitis (AS‐AIH) is characterized by rapid progression and poor prognosis, with a current lack of effective targeted treatments. Stem cell therapy has demonstrated significant therapeutic promise across various diseases. However, the intricate pathogenesis AS‐AIH hindered widespread utilization mesenchymal stem cells (MSCs) in this domain. Herein, it that necroptosis, as primary mode death AIH, crucial causing AS‐AIH. Inflammatory macrophages are population involved necroptosis. Inhibition specificity protein 1/sphingosine kinase 1/sphingosine‐1‐phosphate (SP1/SK1/S1P) axis responsible for phenomenon, leading to excessive activation intrahepatic immune system aggravating liver damage. Furthermore, S1P/S1PR2/YAP key pathway initiating regeneration during S1P synthesized hepatocytes source, process also regulated SP1/SK1 axis. MSCs promote synthesis through delivery SP1, which inhibits necroptosis synergistically enhances regeneration. In addition, same mechanism, further aiding These findings unveil core provide theoretical foundation using potential modality.

Язык: Английский

Процитировано

1
Anion exchange regulated charge separation engineering in bismuth nanoflowers for sonocatalytic radio-immunotherapy DOI
Hong Qian, Junjie Pan, Xueyu Li

и другие.

Journal of Colloid and Interface Science, Год журнала: 2025, Номер 687, С. 801 - 816

Опубликована: Фев. 17, 2025

Язык: Английский

Процитировано

1
Interleukin-1α release during necrotic-like cell death generates myeloid-driven immunosuppression that restricts anti-tumor immunity DOI
Kay Hänggi, Jie Li, Achintyan Gangadharan

и другие.

Cancer Cell, Год журнала: 2024, Номер unknown

Опубликована: Ноя. 1, 2024

Язык: Английский

Процитировано

6