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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
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We are analyzing https://link.springer.com/article/10.1007/s11010-025-05281-4.

Title:
Decoding STING’s roles in cancer: immunity, pain, dormancy, and autophagy | Molecular and Cellular Biochemistry
Description:
Stimulator of interferon genes (STING) is ubiquitously localized in the endoplasmic reticulum of diverse cell types, serving as a cornerstone of the cyclic GMP–AMP synthase (cGAS)–STING signaling pathway, which is critical for detecting cytosolic DNA and initiating innate immune responses. Conventionally, researchers have characterized STING as a tumor suppressor; however, emerging evidence indicates that activating STING may also facilitate tumor progression. Notably, the tumor-suppressive and tumor-promoting effects mediated by STING are highly context dependent and influenced by specific tumor types and stages. Beyond its central role in immune defense, the STING signaling pathway regulates various physiological and pathological processes within cells. Dormant tumor cells, for instance, can adjust their STING expression to evade immune detection and clearance. Additionally, STING-induced autophagy functions as a negative regulator of STING, establishing a reciprocal interplay that impacts both innate immunity and antitumor immunity. Furthermore, STING activation can simultaneously stimulate the production of proinflammatory and anti-inflammatory cytokines, underscoring its dualistic impact on cancer pain modulation. Therefore, a nuanced understanding of STING’s immunoregulatory and alternative roles in antitumor immunity is essential for effectively designing STING-targeted cancer therapies. This review comprehensively analyzes STING’s structure and function, systematically elucidating its mechanisms and roles in antitumor immunity, dormancy, autophagy, and cancer pain modulation. By integrating current insights, this work aims to establish a robust theoretical foundation for advancing the development and clinical implementation of STING-targeted cancer therapies.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Health & Fitness
  • Business & Finance

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {šŸ’ø}

We don't see any clear sign of profit-making.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {šŸ”}

pubmed, article, google, scholar, cas, central, cancer, sting, cell, wang, zhang, httpsdoiorgs, chen, liu, tumor, yang, nat, autophagy, immunity, pathway, cells, activation, cgassting, antitumor, signaling, immunol, pain, immune, nature, lee, sci, dna, immunotherapy, sun, interferon, rev, zhao, kim, mol, commun, rep, type, res, tumors, tang, promotes, response, zhou, dormancy, microenvironment,

Topics {āœ’ļø}

stat3-sting-ifn axis controls month download article/chapter sting-mediated t-cell activation sting-mediated ifn-α production sting-mediated interferon-β signaling sting-triggered tumor-migrating neutrophils cgas-activated endothelial cell stimulates anti-tumor immunity host dna-sensing pathway tumor-derived cgamp triggers tgf-β signaling pathways ifnα-induced bst2+ tumor tax1bp1-dependent autophagic degradation type-ii-interferon-mediated signalling anti-tumor immune response tumor-promoting effects mediated sting-targeted cancer therapies cell-mediated tumor immunity interferon-dependent antitumor immunity cgas-sting signaling axis ifn-dependent monocyte reprogramming interleukin-6-mediated functional upregulation enhance anti-tumor immunotherapy chronic cancer-related pain cytotoxic t-cell activity lats2/vgll3 hippo signaling intraperitoneal vascular-immune microenvironment cyclic gmp–amp synthase cyclic gmp-amp synthase cancer-induced bone pain cgas-sting-ifnβ-hla sting-induced autophagy functions microbiota triggers sting-type cytosolic dna sensing bridging cgas-sting pathway sting-mediated interferon response cytosolic dna sensor sting-activating nanoparticles normalize interferon-stimulated gene sting cancer cell-derived type activating cgas-sting pathway nampt-driven m2 polarization targeting cgas-sting pathway interferons nf-Īŗb triple-negative breast cancer jak/pi3k signaling pathway xin-hua liang ya-ling tang autophagy-related pathways tumor cell-intrinsic expression

Schema {šŸ—ŗļø}

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         headline:Decoding STING’s roles in cancer: immunity, pain, dormancy, and autophagy
         description:Stimulator of interferon genes (STING) is ubiquitously localized in the endoplasmic reticulum of diverse cell types, serving as a cornerstone of the cyclic GMP–AMP synthase (cGAS)–STING signaling pathway, which is critical for detecting cytosolic DNA and initiating innate immune responses. Conventionally, researchers have characterized STING as a tumor suppressor; however, emerging evidence indicates that activating STING may also facilitate tumor progression. Notably, the tumor-suppressive and tumor-promoting effects mediated by STING are highly context dependent and influenced by specific tumor types and stages. Beyond its central role in immune defense, the STING signaling pathway regulates various physiological and pathological processes within cells. Dormant tumor cells, for instance, can adjust their STING expression to evade immune detection and clearance. Additionally, STING-induced autophagy functions as a negative regulator of STING, establishing a reciprocal interplay that impacts both innate immunity and antitumor immunity. Furthermore, STING activation can simultaneously stimulate the production of proinflammatory and anti-inflammatory cytokines, underscoring its dualistic impact on cancer pain modulation. Therefore, a nuanced understanding of STING’s immunoregulatory and alternative roles in antitumor immunity is essential for effectively designing STING-targeted cancer therapies. This review comprehensively analyzes STING’s structure and function, systematically elucidating its mechanisms and roles in antitumor immunity, dormancy, autophagy, and cancer pain modulation. By integrating current insights, this work aims to establish a robust theoretical foundation for advancing the development and clinical implementation of STING-targeted cancer therapies.
         datePublished:2025-04-24T00:00:00Z
         dateModified:2025-04-24T00:00:00Z
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            Cancer Research
            Medical Biochemistry
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      description:Stimulator of interferon genes (STING) is ubiquitously localized in the endoplasmic reticulum of diverse cell types, serving as a cornerstone of the cyclic GMP–AMP synthase (cGAS)–STING signaling pathway, which is critical for detecting cytosolic DNA and initiating innate immune responses. Conventionally, researchers have characterized STING as a tumor suppressor; however, emerging evidence indicates that activating STING may also facilitate tumor progression. Notably, the tumor-suppressive and tumor-promoting effects mediated by STING are highly context dependent and influenced by specific tumor types and stages. Beyond its central role in immune defense, the STING signaling pathway regulates various physiological and pathological processes within cells. Dormant tumor cells, for instance, can adjust their STING expression to evade immune detection and clearance. Additionally, STING-induced autophagy functions as a negative regulator of STING, establishing a reciprocal interplay that impacts both innate immunity and antitumor immunity. Furthermore, STING activation can simultaneously stimulate the production of proinflammatory and anti-inflammatory cytokines, underscoring its dualistic impact on cancer pain modulation. Therefore, a nuanced understanding of STING’s immunoregulatory and alternative roles in antitumor immunity is essential for effectively designing STING-targeted cancer therapies. This review comprehensively analyzes STING’s structure and function, systematically elucidating its mechanisms and roles in antitumor immunity, dormancy, autophagy, and cancer pain modulation. By integrating current insights, this work aims to establish a robust theoretical foundation for advancing the development and clinical implementation of STING-targeted cancer therapies.
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      dateModified:2025-04-24T00:00:00Z
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         Cancer Research
         Medical Biochemistry
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External Links {šŸ”—}(1000)

Analytics and Tracking {šŸ“Š}

  • Google Tag Manager

Libraries {šŸ“š}

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CDN Services {šŸ“¦}

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