Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1080/07391102.2016.1264887 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Sevoflurane postconditioning mitigates neuronal hypoxic-ischemic injury via regulating reactive astrocytic STAT3 protein modification.
Chem Biol Interact
January 2025
Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, 110004, China. Electronic address:
Astrocyte activation plays a pivotal role in accelerating the cascade of neuroinflammation associated with the development of hypoxic-ischemic brain injury. This study aimed to investigate the mechanism by which sevoflurane postconditioning mitigates neuronal damage through astrocytes by regulating reactive astrocytic Signal Transducer and Activator of Transcription 3 (STAT3) modifications. A modified Rice‒Vannucci model in rats and a conditioned culture system established by subjecting primary astrocytes to oxygen glucose deprivation, followed by using the conditioned medium to culture the neuron cell line SH-SY5Y were used to simulate HI insult in vivo and in vitro, respectively.
View Article and Find Full Text PDFThe LINC00319 binding to STAT3 promotes the cell proliferation, migration, invasion and EMT process in oral squamous cell carcinoma.
Arch Biochem Biophys
November 2024
Stomatological Hospital, School of Stomatology, Southern Medical University, S366 Jiangnan Boulevard, Haizhu District, Guangzhou 510280, Guangdong Province, China. Electronic address:
Article Synopsis
- LINC00319 is a long non-coding RNA that has been linked to the progression of oral squamous cell carcinoma (OSCC) and is known to be involved in regulatory processes like the competing endogenous RNA (ceRNA) mechanism.
- This study aimed to investigate LINC00319's role in OSCC and its potential interactions with the STAT3 signaling pathway, providing insights into new regulatory mechanisms that could serve as therapeutic targets.
- Results showed that LINC00319 is upregulated in OSCC and enhances tumor progression by directly binding to and activating STAT3 signaling, with in vivo models confirming its role in tumor growth and STAT3 activation.
Trichinellaspiralis C-type lectin mediates larva invasion of gut mucosa via binding to syndecan-1 and damaging epithelial integrity in mice.
Int J Biol Macromol
November 2024
Department of Parasitology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, China. Electronic address:
Article Synopsis
- C-type lectin (CTL) is crucial for how the T. spiralis parasite attaches to and invades intestinal cells while evading the immune system.
- The study found that recombinant T. spiralis CTL (rTsCTL) binds to a protein called syndecan-1, which leads to damage in intestinal cell integrity, promotes parasite invasion, and increases inflammation.
- Using inhibitors against syndecan-1 and the STAT3 pathway reduced parasite invasion, lowered inflammation, and improved gut health in infected mice, suggesting that TsCTL could be a potential target for vaccines against T. spiralis infection.
Hepatocellular carcinoma (HCC), a highly lethal solid tumor, has shown responsiveness to ferroptosis inducers, presenting new avenues in cancer treatment. Our study focuses on the roles of STAT3 and Nf-κB in regulating ferroptosis, particularly their interaction in this process. Using HepG2 cells, we employed specific inhibitors (Stattic for STAT3 and Bay11-7082 for Nf-κB) and a ferroptosis inducer, SSPH I, to dissect their collective impact on ferroptosis.
View Article and Find Full Text PDFIntegrin αVβ1-activated PYK2 promotes the progression of non-small-cell lung cancer via the STAT3-VGF axis.
Cell Commun Signal
June 2024
Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Background: Non-small-cell lung cancer (NSCLC) accounts for 80-85% of all lung cancer and is the leading cause of cancer-related deaths globally. Although various treatment strategies have been introduced, the 5-year survival rate of patients with NSCLC is only 20-30%. Thus, it remains necessary to study the pathogenesis of NSCLC and develop new therapeutic drugs.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!