This study aimed to investigate the role and regulatory mechanism of RNF126 in nasopharyngeal carcinoma. Firstly, the expression and prognosis of RNF126 were analyzed by TCGA database. The expression of RNF126 was further verified by NPC tissue samples and cells. An ectopic xenograft model was constructed to verify the regulatory role of RNF126 in NPC tumor progression. The regulatory effect of RNF126 on macrophage polarization and migration was verified by co-culture of tumor cells and THP-1 cells. The role of RNF126 in tumor exosomes involved in intercellular communication was further verified by nanoparticle tracking technology, western blotting and immunofluorescence assays. QRT-PCR, half-life assay and WB assay were used to verify the regulatory effect of RNF126 on PTEN ubiquitination and PI3K/AKT pathway. Finally, an in vivo assay was used to verify the regulation of exosomes on tumor growth and metastasis. In summary, we found for the first time that tumor-derived exosomal PTEN degrades PTEN through ubiquitination to regulate the tumor immune microenvironment and promote NPC growth and metastasis. These results provide the basis for the screening of early markers of NPC and targeted therapy.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10495-022-01738-9 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Glucose-6-phosphate dehydrogenase regulates mitophagy by maintaining PINK1 stability.
Life Metab
February 2025
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.
Glucose-6-phosphate dehydrogenase (G6PD) is the rate-limiting enzyme in the pentose phosphate pathway (PPP) in glycolysis. Glucose metabolism is closely implicated in the regulation of mitophagy, a selective form of autophagy for the degradation of damaged mitochondria. The PPP and its key enzymes such as G6PD possess important metabolic functions, including biosynthesis and maintenance of intracellular redox balance, while their implication in mitophagy is largely unknown.
View Article and Find Full Text PDFA novel strategy for the protective effect of ginsenoside Rg1 against ovarian reserve decline by the PINK1 pathway.
Pharm Biol
December 2025
The Affiliated Hospital, Changchun University of Chinese Medicine, Changchun, China.
Context: The decline in ovarian reserve is a major concern in female reproductive health, often associated with oxidative stress and mitochondrial dysfunction. Although ginsenoside Rg1 is known to modulate mitophagy, its effectiveness in mitigating ovarian reserve decline remains unclear.
Objective: To investigate the role of ginsenoside Rg1 in promoting mitophagy to preserve ovarian reserve.
Feedback loop centered on MAF1 reduces blood-brain barrier damage in sepsis-associated encephalopathy.
Cell Mol Biol Lett
January 2025
Department of Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Background: A previous study found that MAF1 homolog, a negative regulator of RNA polymerase III (MAF1), protects the blood-brain barrier (BBB) in sepsis-associated encephalopathy (SAE); however, the related molecular mechanisms remain unclear.
Subjects And Methods: In this study, a rat sepsis model was constructed using the cecum ligation and puncture (CLP) method. In vitro, rat brain microvascular endothelial cells and astrocytes were stimulated with serum from the sepsis model rats.
Male sex determination maintains proteostasis and extends lifespan of daf-18/PTEN deficient C. elegans.
EMBO Rep
January 2025
The Zhongzhou Laboratory for Integrative Biology, Henan University, 450000, Zhengzhou, Henan, China.
Although females typically have a survival advantage, those with PTEN functional abnormalities face a higher risk of developing tumors than males. However, the differences in how each sex responds to PTEN dysfunction have rarely been studied. We use Caenorhabditis elegans to investigate how male and hermaphrodite worms respond to dysfunction of the PTEN homolog daf-18.
View Article and Find Full Text PDFUBE2S, downregulated by miR-152-3p, facilitates prostate cancer progression through the PTEN-mediated AKT/mTOR pathway.
Hum Mol Genet
January 2025
Departments of Urology, Affiliated Hospital of Chifeng University, No. 42 Wangfu Street, 024000, Chifeng, China.
Objectives: In recent years, the incidence and mortality rates of prostate cancer (PCa) have still not been significantly reduced and the mechanisms of tumor onset and progression are still not fully understood. The pathogenic mechanisms and upstream regulation of UBE2S expression in prostate cancer have not been elucidated.
Methods: Here, we performed bioinformatic analysis of public databases to reveal the expression of UBE2S in PCa and its association with Gleason score, tumor staging, biochemical recurrence, and survival.
Want 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!