Background: Exosomal long non-coding RNA (lncRNA) has been shown to be potential biomarker for cancer diagnosis and follow up. However, little is known about its application in esophageal squamous cell carcinoma (ESCC) detection. Here, we sought to develop a novel diagnostic model based on serum exosomal lncRNAs to improve ESCC screening efficiency.

Methods: A multiphase, case-control study was conducted among 140 ESCC patients and 140 healthy controls. Microarray screening was performed to acquire differentially expressed exosomal lncRNAs in the discovery phase. The diagnostic model Index I was constructed based on a panel of three lncRNAs using logistic regression in the training phase, and were confirmed in a subsequent validation phase. A receiver operating characteristic (ROC) curve was generated to calculate the diagnostic value. The effects of the selected lncRNAs level on ESCC mortality were evaluated using a Cox hazard regression model and Kaplan-Meier curve analysis, and the expression level with clinicopathological features was also calculated. Finally, we explored the oncogenic potential of candidate lncRNA RASSF8-AS1 in vitro and by target mRNA sequencing.

Results: Index I was able to discriminate ESCC patients from healthy controls, and showed superiority to classic tumor biomarkers. Moreover, serum levels of the exosomal lncRNAs correlated with clinicopathological features and prognosis. The in vitro assays showed that RASSF8-AS1 played an oncogenic role in ESCC. Target mRNA scanning results suggested involvement of RASSF8-AS1 in tumor immunity and metabolism.

Conclusion: The newly identified serum exosomal lncRNAs could be used as new biomarkers for ESCC, and showed oncogenic potential in ESCC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9715784PMC
http://dx.doi.org/10.1111/1759-7714.14690DOI Listing

Publication Analysis

Top Keywords

exosomal lncrnas
20
esophageal squamous
8
squamous cell
8
cell carcinoma
8
escc
8
diagnostic model
8
serum exosomal
8
escc patients
8
healthy controls
8
clinicopathological features
8

Similar Publications

Biofluid-Derived Exosomal LncRNAs: Their Potential in Obesity and Related Comorbidities.

Biology (Basel)

November 2024

Zhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan 528400, China.

Obesity has escalated into a critical global health crisis, tripling in prevalence since the mid-1970s. This increase mirrors the rise in metabolic-associated diseases such as type 2 diabetes (T2D) and its complications, certain cancers, and cardiovascular conditions. While substantial research efforts have enriched our understanding and led to the development of innovative management strategies for these diseases, the suboptimal response rates of existing therapies remain a major obstacle to effectively managing obesity and its associated conditions.

View Article and Find Full Text PDF

Exosomal circ_0006896 promotes AML progression via interaction with HDAC1 and restriction of antitumor immunity.

Mol Cancer

January 2025

Department of Hematology, Qilu Hospital of Shandong University, No.117, West of Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.

Background: Drug resistance and immune escape continue to contribute to poor prognosis in AML. Increasing evidence suggests that exosomes play a crucial role in AML immune microenvironment.

Methods: Sanger sequencing, RNase R and fluorescence in situ hybridization were performed to confirm the existence of circ_0006896.

View Article and Find Full Text PDF

[Roles of ferroptosis in the development of diabetic nephropathy].

Zhejiang Da Xue Xue Bao Yi Xue Ban

December 2024

Department of Endocrinology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610072, China.

Article Synopsis
  • Diabetic nephropathy is a serious complication of diabetes that can lead to death, and ferroptosis (an iron-dependent cell death process) plays a role in its progression.
  • AMPK signaling can slow down diabetic nephropathy but excessive activation may cause autophagic death, while Nrf2 and HO-1 pathways can protect against ferroptosis; however, these pathways have complex effects.
  • Other factors like TGF-β1 and specific exosome-related signals also contribute to the development of diabetic nephropathy, suggesting potential new therapeutic targets to prevent or treat this condition.
View Article and Find Full Text PDF

Transcriptional profiling of exosomes derived from serum of patients with rare earth pneumoconiosis by RNA-sequencing and PI3K/Akt pathway is activated in lung of mice exposed to rare earth NdO.

Toxicol Lett

January 2025

Department of Public Health,International College,Krirk University, Bangkok 10220, Thailand; School of Public Health, Baotou Medical College, Baotou 014030, Inner Mongolia, PR China. Electronic address:

Rare earth is used extensively around the world, and rare earth particles cause a respiratory disease in workers termed rare earth pneumoconiosis(REP) that have attracted considerable attention. However, the mechanisms of REP, characterized by diffuse pulmonary fibrosis, are elusive. REP progression involves various signaling pathway networks comprising numerous cell types and cytokines.

View Article and Find Full Text PDF

Alzheimer's disease (AD) is a neurodegenerative disease that primarily affects the elderly population and is the leading cause of dementia. Meanwhile, the vascular hypothesis suggests that vascular damage occurs in the early stages of the disease, leading to neurodegeneration and hindered waste clearance, which in turn triggers a series of events including the accumulation of amyloid plaques and Tau protein tangles. Non-coding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), have been found to be involved in the regulation of AD.

View Article and Find Full Text PDF

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!