Oncogenic functions and therapeutic potentials of targeted inhibition of SMARCAL1 in small cell lung cancer DOI
Beibei Sun, Guizhen Wang,

Si-Chong Han

et al.

Cancer Letters, Journal Year: 2024, Volume and Issue: 592, P. 216929 - 216929

Published: April 30, 2024

Language: Английский

The hallmarks of cancer immune evasion DOI
Claudia Galassi, Timothy A. Chan, Ilio Vitale

et al.

Cancer Cell, Journal Year: 2024, Volume and Issue: 42(11), P. 1825 - 1863

Published: Oct. 10, 2024

Language: Английский

Citations

78

The balance of STING signaling orchestrates immunity in cancer DOI

Klara Rasmussen Bollerup Lanng,

Emil Leth Lauridsen,

Martin R. Jakobsen

et al.

Nature Immunology, Journal Year: 2024, Volume and Issue: 25(7), P. 1144 - 1157

Published: June 25, 2024

Language: Английский

Citations

44

Epigenetic regulation of tumor immunity DOI Creative Commons
Lizhi Pang, Fei Zhou, Yang Liu

et al.

Journal of Clinical Investigation, Journal Year: 2024, Volume and Issue: 134(12)

Published: June 16, 2024

Although cancer has long been considered a genetic disease, increasing evidence shows that epigenetic aberrations play crucial role in affecting tumor biology and therapeutic response. The dysregulated epigenome cells reprograms the immune landscape within microenvironment, thereby hindering antitumor immunity, promoting progression, inducing immunotherapy resistance. Targeting epigenetically mediated tumor-immune crosstalk is an emerging strategy to inhibit progression circumvent limitations of current immunotherapies, including checkpoint inhibitors. In this Review, we discuss mechanisms by which regulate interactions how targeted therapies synergize with immunotherapy.

Language: Английский

Citations

8

Mechanisms and regulation of replication fork reversal DOI Creative Commons
Madison B. Adolph,

David Cortez

DNA repair, Journal Year: 2024, Volume and Issue: 141, P. 103731 - 103731

Published: July 22, 2024

DNA replication is remarkably accurate with estimates of only a handful mutations per human genome cell division cycle. Replication stress caused by lesions, transcription-replication conflicts, and other obstacles to the machinery must be efficiently overcome in ways that minimize errors maximize completion synthesis. fork reversal one mechanism helps cells tolerate stress. This process involves reannealing parental template strands generation nascent-nascent duplex. While may beneficial facilitating repair or switching, it confined appropriate contexts preserve stability. Many enzymes have been implicated this including ATP-dependent translocases like SMARCAL1, ZRANB3, HLTF, helicase FBH1. In addition, RAD51 recombinase required. additional factors regulatory activities also act ensure instead yielding undesirable outcomes. Finally, reversed forks stabilized often need restarted complete Disruption deregulation causes variety diseases. review we will describe latest models for key mechanisms regulation.

Language: Английский

Citations

8

Circ_0001947 encapsulated by small extracellular vesicles promotes gastric cancer progression and anti-PD-1 resistance by modulating CD8+ T cell exhaustion DOI Creative Commons
Bingyu Wang, Wenbo Liu, Mingming Zhang

et al.

Journal of Nanobiotechnology, Journal Year: 2024, Volume and Issue: 22(1)

Published: Sept. 14, 2024

Language: Английский

Citations

6

Tumor Microenvironment Targeted by Polysaccharides in Cancer Prevention: Expanding Roles of Gut Microbiota and Metabolites DOI
Shuai Han, Yixin Luo, Zuomin Hu

et al.

Molecular Nutrition & Food Research, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 5, 2025

ABSTRACT Since the development of immune checkpoint inhibitors (ICIs), immunotherapy has been widely used as a novel cancer treatment. However, efficacy tumor is largely dependent on microenvironment (TME). The high degree heterogeneity within TME remains major obstacle to acquire satisfactory therapeutic. Emerging studies suggest that gut microbiota becoming an important regulator TME. Polysaccharides immunotherapeutic agents or adjuvants not only exhibit antitumor activity by targeting microbiota, but also expand their role in remodeling To date, mechanism which polysaccharides for prevention via deeply investigated. In this review, recent advances regulation through were systematically outlined, and challenges possible solutions clinical application TME‐targeted discussed. Exploring relationship between from perspective may provide new ideas immunotherapy. This area with deserve further exploration.

Language: Английский

Citations

0

Inflammasome activation in melanoma progression: the latest update concerning pathological role and therapeutic value DOI

Nakaraj Pluetrattanabha,

Thanyaporn Direksunthorn, Irfan Ahmad

et al.

Archives of Dermatological Research, Journal Year: 2025, Volume and Issue: 317(1)

Published: Jan. 16, 2025

Language: Английский

Citations

0

Global trends and emerging insights in BRAF and MEK inhibitor resistance in melanoma: a bibliometric analysis DOI Creative Commons
Jianhao Bai,

Zhongqi Wan,

Wanru Zhou

et al.

Frontiers in Molecular Biosciences, Journal Year: 2025, Volume and Issue: 12

Published: Jan. 17, 2025

This study aims to perform a comprehensive bibliometric analysis of global research on BRAF and MEK inhibitor resistance in melanoma, identifying key trends, influential contributors, emerging themes from 2003 2024. A systematic search was conducted the Web Science Core Collection (WoSCC) database retrieve publications related 1 January 2003, September Bibliometric analyses, including publication citation networks, keyword co-occurrence patterns, were performed using VOSviewer CiteSpace. Collaborative co-cited references, burst analyses mapped uncover shifts focus cooperation. total 3,503 documents, 2,781 articles 722 review papers, analyzed, highlighting significant growth this field. The United States, China, Italy led volume impact, with Harvard University California System among top contributing institutions. Research output showed three phases growth, peaking 2020. Keyword co-citation revealed transition early mutations MAPK pathway activation recent emphasis immunotherapy, combination therapies, non-apoptotic cell death mechanisms like ferroptosis pyroptosis. These trends reflect evolving priorities innovative approaches shaping field inhibitors melanoma. has evolved significantly. provides strategic framework for future investigations, guiding development innovative, multi-modal improve treatment outcomes melanoma patients.

Language: Английский

Citations

0

Jumonji domain-containing protein 6 promotes gastric cancer progression: Modulating immune evasion through autophagy and oxidative stress pathways DOI Open Access
Xinyue Zhang, Na Di

CytoJournal, Journal Year: 2025, Volume and Issue: 22, P. 6 - 6

Published: Jan. 23, 2025

Objective: Immune response is crucial in the development of gastric cancer (GC), and Jumonji domain-containing protein 6 (JMJD6) plays an important role mediating GC cell behavior. This study aims to elucidate mechanisms through which JMJD6 affects autophagy immune evasion cells. Material Methods: Immunocytochemistry was employed assess programmed death-ligand 1 (PD-L1) levels line (MKN-45) epithelial MKN-45 cells with knockdown overexpression were generated. The effect on evaluated using counting kit-8 assay, cellular fluorescence staining, Transwell assays. Western blot analysis immunofluorescence techniques investigate regulation by JMJD6. Reactive oxygen species (ROS) applying ROS staining. Meanwhile, gene expression molecules related antioxidant stress responses assessed assays quantitative real-time polymerase chain reactions, respectively. Results: PD-L1 elevated ( P < 0.001). enhanced migration, invasion, colony formation vitro In cells, epithelial-mesenchymal transition promoted upregulation but notably inhibited increased Sequestosome 1, Microtubule-associated 1A/1B-light 3 (LC3)II/LC3I, activation further addition, reduced production response, reverse effects observed Conclusion: facilitates progression modulating oxidative pathways.

Language: Английский

Citations

0

Transketolase promotes osteosarcoma progression through the YY1PAK4 axis DOI Open Access
Doudou Jing, Wei Wu, Xin Huang

et al.

FEBS Journal, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 23, 2025

Osteosarcoma, a malignant bone tumor that occurs in adolescents, proliferates and is prone to pulmonary metastasis. Osteosarcoma characterized by high genotypic heterogeneity, making it difficult identify reliable anti‐osteosarcoma targets. The genotype of osteosarcoma may be highly dynamic, but its dependence on energy remains constant. Fortunately, tumors tend have relatively consistent metabolic types. Targeting metabolism with anti‐tumor therapies new strategy for treating tumors. Genes related carbohydrate are widely expressed tissues. Transketolase (TKT), key enzyme at the non‐oxidative stage pentose phosphate pathway, up‐regulated various In present study, TKT promoted cell proliferation non‐metabolically. Specifically, bound directly amino acid residues Yin Yang 1 (YY1) acids 201–228, stimulating YY1 bind promoter P21 activated kinase 4 (PAK4) resulting PAK4 expression activation phosphoinositide 3‐kinase‐Akt signaling pathway. Additionally, we designed peptide, YY1‐PEP, based exact mechanism how promotes osteosarcoma. Per vivo vitro experiments, YY1‐PEP displayed properties. study provides feasible against progression.

Language: Английский

Citations

0