ITCH inhibits alkaliptosis in human pancreatic cancer cells through YAP1-dependent SLC16A1 activation DOI

Xiutao Cai,

Fangquan Chen, Hu Tang

et al.

The International Journal of Biochemistry & Cell Biology, Journal Year: 2024, Volume and Issue: 175, P. 106646 - 106646

Published: Aug. 23, 2024

Language: Английский

Targeting paraptosis in cancer: opportunities and challenges DOI Open Access
Fangquan Chen, Hu Tang,

Xiutao Cai

et al.

Cancer Gene Therapy, Journal Year: 2024, Volume and Issue: 31(3), P. 349 - 363

Published: Jan. 4, 2024

Language: Английский

Citations

14

Emerging role of immunogenic cell death in cancer immunotherapy DOI Creative Commons

Kei‐ichiro Arimoto,

Sayuri Miyauchi,

Mengdan Liu

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: May 10, 2024

Cancer immunotherapy, such as immune checkpoint blockade (ICB), has emerged a groundbreaking approach for effective cancer treatment. Despite its considerable potential, clinical studies have indicated that the current response rate to immunotherapy is suboptimal, primarily attributed low immunogenicity in certain types of malignant tumors. Immunogenic cell death (ICD) represents form regulated (RCD) capable enhancing tumor and activating tumor-specific innate adaptive responses immunocompetent hosts. Therefore, gaining deeper understanding ICD evolution crucial developing more therapeutic strategies. This review focuses exclusively on both historical recent discoveries related modes their mechanistic insights, particularly within context immunotherapy. Our findings are also highlighted, revealing mode induction facilitated by atypical interferon (IFN)-stimulated genes (ISGs), including polo-like kinase 2 ( PLK2 ), during hyperactive type I IFN signaling. The concludes discussing potential ICD, with special attention relevance preclinical settings field

Language: Английский

Citations

14

Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases DOI
Zhibo Yang,

Ridong Feng,

Zhao Hai

et al.

APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(9-10), P. 1330 - 1360

Published: July 16, 2024

Language: Английский

Citations

12

Disulfidptosis: A new type of cell death DOI Creative Commons
Fei Xiao, Huili Li, Bei Yang

et al.

APOPTOSIS, Journal Year: 2024, Volume and Issue: unknown

Published: June 17, 2024

Abstract Disulfidptosis is a novel form of cell death that distinguishable from established programmed pathways such as apoptosis, pyroptosis, autophagy, ferroptosis, and oxeiptosis. This process characterized by the rapid depletion nicotinamide adenine dinucleotide phosphate (NADPH) in cells high expression solute carrier family 7 member 11 (SLC7A11) during glucose starvation, resulting abnormal cystine accumulation, which subsequently induces andabnormal disulfide bond formation actin cytoskeleton proteins, culminating network collapse disulfidptosis. review aimed to summarize underlying mechanisms, influencing factors, comparisons with traditional pathways, associations related diseases, application prospects, future research directions

Language: Английский

Citations

9

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

Guoqian Liu

et al.

Journal of Hematology & Oncology, Journal Year: 2025, Volume and Issue: 18(1)

Published: Jan. 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

Language: Английский

Citations

1

Alkaliptosis induction counteracts paclitaxel‐resistant ovarian cancer cells via ATP6V0D1‐mediated ABCB1 inhibition DOI
Fangquan Chen, Junhao Lin, Rui Kang

et al.

Molecular Carcinogenesis, Journal Year: 2024, Volume and Issue: 63(8), P. 1515 - 1527

Published: May 15, 2024

Abstract Paclitaxel serves as the cornerstone chemotherapy for ovarian cancer, yet its prolonged administration frequently culminates in drug resistance, presenting a substantial challenge. Here we reported that inducing alkaliptosis, rather than apoptosis or ferroptosis, effectively overcomes paclitaxel resistance. Mechanistically, ATPase H + transporting V0 subunit D1 (ATP6V0D1), key regulator of plays pivotal role by mediating downregulation ATP‐binding cassette subfamily B member 1 (ABCB1), multidrug resistance protein. Both ATP6V0D1 overexpression through gene transfection and pharmacological enhancement protein stability using JTC801 inhibit ABCB1 upregulation, resulting growth inhibition drug‐resistant cells. Additionally, increasing intracellular pH to alkaline (pH 8.5) via sodium hydroxide application suppresses expression, whereas reducing acidic conditions 6.5) with hydrochloric acid amplifies expression Collectively, these results indicate potentially effective therapeutic strategy targeting paclitaxel‐resistant cancer ATP6V0D1‐dependent alkaliptosis.

Language: Английский

Citations

8

Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma DOI Creative Commons
Qingshui Wang, Jiamin Liu,

Ruiqiong Li

et al.

Cancer Cell International, Journal Year: 2024, Volume and Issue: 24(1)

Published: May 10, 2024

Abstract Kidney Clear Cell Carcinoma (KIRC), the predominant form of kidney cancer, exhibits a diverse therapeutic response to Immune Checkpoint Inhibitors (ICIs), highlighting need for predictive models ICI efficacy. Our study has constructed prognostic model based on 13 types Programmed Death (PCD), which are intertwined with tumor progression and immune microenvironment. Validated by analyses comprehensive datasets, this identifies seven key PCD genes that delineate two subtypes distinct profiles sensitivities anti-PD-1 therapy. The high-PCD group demonstrates more immune-suppressive environment, while low-PCD shows better responses PD-1 treatment. In particular, TOP2A emerged as crucial, its inhibition markedly reducing KIRC cell growth mobility. These findings underscore relevance PCDs in predicting outcomes immunotherapy response, implications enhancing clinical decision-making.

Language: Английский

Citations

6

Macropinocytosis inhibits alkaliptosis in pancreatic cancer cells through fatty acid uptake DOI
Fangquan Chen, Hu Tang, Junhao Lin

et al.

Carcinogenesis, Journal Year: 2024, Volume and Issue: unknown

Published: July 14, 2024

Alkaliptosis, a form of regulated cell death, is characterized by lysosomal dysfunction and intracellular pH alkalinization. The pharmacological induction alkaliptosis using the small molecule compound JTC801 has emerged as promising anticancer strategy in various types cancers, particularly pancreatic ductal adenocarcinoma (PDAC). In this study, we investigate novel mechanism which macropinocytosis, an endocytic process involving uptake extracellular material, promotes resistance to human PDAC cells. Through lipid metabolomics analysis functional studies, demonstrate that inhibition fatty acids, such oleic acid, not dependent on endogenous synthetic pathways but rather exogenous facilitated macropinocytosis. Consequently, targeting macropinocytosis through approaches (e.g., EIPA or EHoP-016) genetic interventions RAC1 knockdown) effectively enhances JTC801-induced These findings provide compelling evidence modulation can increase sensitivity cancer cells inducers.

Language: Английский

Citations

4

Sphingolipid metabolism and regulated cell death in malignant melanoma DOI
Kexin Yan, Mengli Zhang, Hao Song

et al.

APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(11-12), P. 1860 - 1878

Published: July 28, 2024

Language: Английский

Citations

4

Intracellular metal ion-based chemistry for programmed cell death DOI
Y You, Zhongying Guo, Tyler Wolter

et al.

Chemical Society Reviews, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Intracellular metal ions play essential roles in multiple physiological processes, including catalytic action, diverse cellular intracellular signaling, and electron transfer. It is crucial to maintain ion homeostasis which achieved by the subtle balance of storage release intracellularly along with influx efflux at interface cell membrane. Dysregulation has been identified as a key mechanism triggering programmed death (PCD). Despite importance initiating PCD, molecular mechanisms within these processes are infrequently discussed. An in-depth understanding review role PCD may better uncover novel tools for cancer diagnosis therapy. Specifically, calcium (Ca

Language: Английский

Citations

0