<i>STIL</i> enhances the development of lung adenocarcinoma by regulating the glycolysis pathway DOI Creative Commons
Lei Wang,

XIANJIN XIE

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics, Journal Year: 2024, Volume and Issue: 33(1), P. 123 - 132

Published: May 29, 2024

Background: To investigate STIL centriolar assembly protein (STIL)'s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined E2 promoter binding factor 1 (E2F1) expressions their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis (GEPIA).Methods: Functional assays including CCK-8, wound-healing, 5-ethynyl-2-deoxyuridine (EdU), Transwell assays, flow cytometry, elucidated E2F1's effects cell viability, proliferation, apoptosis, migration.GSEA identified potential pathways, while metabolic assessed glucose metabolism.Results: Our findings reveal that E2F1 are overexpressed LUAD, correlating with adverse outcomes.It enhances migration, invasion, suppresses activating downstream of E2F1.Silencing reversed the promotion effect overexpression viability invasiveness.Importantly, modulates glycolysis, influencing consumption, lactate production, energy balance cells.Conclusion: model, incorporating STIL, age, disease stage, robustly predicts patient prognosis, underscoring STIL's pivotal pathogenesis through reprogramming.This comprehensive approach not only confirms value but also highlights its as a therapeutic target LUAD.

Language: Английский

Targeting cGAS-STING pathway for reprogramming tumor-associated macrophages to enhance anti-tumor immunotherapy DOI Creative Commons
Weiyue Zhang, Xin Huang

Biomarker Research, Journal Year: 2025, Volume and Issue: 13(1)

Published: March 12, 2025

Abstract The cyclic GMP-AMP synthase (cGAS)-stimulator interferon genes (STING) signaling pathway plays a crucial role in activating innate and specific immunity anti-tumor immunotherapy. As the major infiltrating cells tumor microenvironment (TME), tumor-associated macrophages (TAMs) could be polarized into either M1 or pro-tumor M2 types based on various stimuli. Accordingly, targeted reprogramming TAMs to restore immune balance shows promise as an effective strategy. In this review, we aim target cGAS-STING for enhance We investigated double-edged sword effects of regulating TME. regulative roles its impact TME were further revealed. More importantly, several strategies targeting designed enhancing Taken together, might promising strategy

Language: Английский

Citations

1
Recent advancements in cGAS-STING activation, tumor immune evasion, and therapeutic implications DOI
Md Saiful Islam, Mohammad Saiful Islam, Mst Rubaiat Nazneen Akhand

et al.

Medical Oncology, Journal Year: 2024, Volume and Issue: 41(11)

Published: Oct. 18, 2024

Language: Английский

Citations

4
STING Agonists and How to Reach Their Full Potential in Cancer Immunotherapy DOI Creative Commons
Laura Gehrcken, Christophe Deben, Evelien Smits

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: March 27, 2025

Abstract As cancer continues to rank among the leading causes of death, demand for novel treatments has never been higher. Immunotherapy shows promise, yet many solid tumors such as pancreatic or glioblastoma remain resistant. In these, “cold” tumor microenvironment with low immune cell infiltration and inactive anti‐tumoral cells leads increased resistance these drugs. This driven development several drug candidates, including stimulators interferon genes (STING) agonists reprogram system fight off tumors. Preclinical studies demonstrated that STING can trigger immunity cycle increase type I secretion T activation, which subsequently induces regression. Despite promising preclinical data, biological physical challenges persist in translating success into clinical trials. Nonetheless, combination strategies are emerging, investigating other immunotherapies, presenting encouraging results. review will examine potential assess benefits employing them immunotherapy.

Language: Английский

Citations

0
Decoding STING’s roles in cancer: immunity, pain, dormancy, and autophagy DOI
Huan‐Xin Lin, Ya‐ling Tang,

Xinhua Liang

et al.

Molecular and Cellular Biochemistry, Journal Year: 2025, Volume and Issue: unknown

Published: April 24, 2025

Language: Английский

Citations

0
Berbamine As Potential STING Inhibitor For KRAS-Mutant Non-Small Cell Lung Cancer DOI Creative Commons
Yan Han, Jumin Huang, Yuwei Wang

et al.

Pharmacological Research, Journal Year: 2025, Volume and Issue: 216, P. 107777 - 107777

Published: May 16, 2025

Lung adenocarcinoma (LUAD) is a leading cause of cancer-related mortality. Poor prognostic results in LUAD are frequently associated with KRAS mutations and drug resistance. can induce STING activation by triggering DNA damage response (DDR) activation. This persistently activated signaling gives rise to an immunosuppressive microenvironment, thereby complicating treatment efforts. In this study, we identified that the low-toxicity pro-apoptotic Berbamine (BBM) as potential therapeutic agent for cells mutations. BBM exhibits anti-tumor effects cell cycle arrest, enhancing senescence, activating apoptosis. also targets STING, downregulation p-STING (Ser366) CCL2. turn reduced infiltration M-MDSCs into tumor microenvironment. These combined mechanisms not only suppress STING-dependent growth but remodel immunity. Collectively, our findings position promising mutations, offering strategy target STING-associated pathways, overcome immune suppression, ultimately improve patient outcomes.

Language: Английский

Citations

0
<i>STIL</i> enhances the development of lung adenocarcinoma by regulating the glycolysis pathway DOI Creative Commons
Lei Wang,

XIANJIN XIE

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics, Journal Year: 2024, Volume and Issue: 33(1), P. 123 - 132

Published: May 29, 2024

Background: To investigate STIL centriolar assembly protein (STIL)'s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined E2 promoter binding factor 1 (E2F1) expressions their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis (GEPIA).Methods: Functional assays including CCK-8, wound-healing, 5-ethynyl-2-deoxyuridine (EdU), Transwell assays, flow cytometry, elucidated E2F1's effects cell viability, proliferation, apoptosis, migration.GSEA identified potential pathways, while metabolic assessed glucose metabolism.Results: Our findings reveal that E2F1 are overexpressed LUAD, correlating with adverse outcomes.It enhances migration, invasion, suppresses activating downstream of E2F1.Silencing reversed the promotion effect overexpression viability invasiveness.Importantly, modulates glycolysis, influencing consumption, lactate production, energy balance cells.Conclusion: model, incorporating STIL, age, disease stage, robustly predicts patient prognosis, underscoring STIL's pivotal pathogenesis through reprogramming.This comprehensive approach not only confirms value but also highlights its as a therapeutic target LUAD.

Language: Английский

Citations

0