Long noncoding RNAs (lncRNAs) have been implicated in tumorigenesis, including lung adenocarcinoma (LUAD). However, the functional and regulatory mechanisms of lncRNAs in LUAD remain poorly understood. In this study, we investigated the role of lncRNA ZBED5-AS1 in LUAD. We found that ZBED5-AS1 was upregulated in LUAD specimens and overexpressed in LUAD cell lines. ZBED5-AS1 promoted LUAD cell proliferation, migration, and invasion in vitro and promoted LUAD cell growth in vivo. ZBED5-AS1 promoted ZNF146 expression, activating the ATR/Chk1 pathway and leading to LUAD progression. We observed that exosomes from LUAD cells have a higher expression of ZBED5-AS1 compared with exosomes from the normal cell line BEAS-2B. Coculture experiments with exosomes showed that ZBED5-AS1 expression was downregulated after coculture with Si-ZBED5-AS1 exosomes, and coculture with exosomes with low ZBED5-AS1 expression inhibited proliferation and invasion of LUAD cells. Our results indicate that ZBED5-AS1 functions as an oncogenic factor in LUAD cells by targeting the ZNF146/ATR/Chk1 axis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10530271PMC
http://dx.doi.org/10.3390/ijms241813925DOI Listing

Publication Analysis

Top Keywords

luad cell
12
luad cells
12
luad
11
zbed5-as1
9
long noncoding
8
lung adenocarcinoma
8
znf146/atr/chk1 axis
8
zbed5-as1 promoted
8
promoted luad
8
zbed5-as1 expression
8

Similar Publications

Interpreting Lung Cancer Health Disparity between African American Males and European American Males.

Proceedings (IEEE Int Conf Bioinformatics Biomed)

December 2024

Knight Foundation School of Computing and Information Sciences, Florida International University, Miami, USA.

Lung cancer remains a predominant cause of cancer-related deaths, with notable disparities in incidence and outcomes across racial and gender groups. This study addresses these disparities by developing a computational framework leveraging explainable artificial intelligence (XAI) to identify both patient- and cohort-specific biomarker genes in lung cancer. Specifically, we focus on two lung cancer subtypes, Lung Adenocarcinoma (LUAD) and Lung Squamous Cell Carcinoma (LUSC), examining distinct racial and sex-specific cohorts: African American males (AAMs) and European American males (EAMs).

View Article and Find Full Text PDF

Background: Lung adenocarcinoma (LUAD) is a highly aggressive tumor with one of the highest morbidity and mortality rates in the world. Nucleotide metabolic processes are critical for cancer development, progression, and alteration of the tumor microenvironment. However, the effect of nucleotide metabolism on LUAD remains to be thoroughly investigated.

View Article and Find Full Text PDF

Introduction: Copine-3 (CPNE3) is a conservative calcium-dependent phospholipid-binding protein belonging to the copines protein family. CPNE3 has been implicated in the development and progression of several diseases, including cancer.

Method: Herein, we investigated the molecular mechanisms through which CPNE3 regulates the migration of lung adenocarcinoma (LUAD) cells in vitro.

View Article and Find Full Text PDF

Polycystic kidney and hepatic disease 1-like protein 1 (PKHD1L1) is predicted to encode a large type I transmembrane protein involved in hearing transmission and mediating cellular immunity under physiological conditions. However, its role in cancer progression, especially in lung adenocarcinoma (LUAD), has not been fully elucidated. In this study, we observed significantly lower expression of PKHD1L1 in LUAD tissues than in normal lung tissues on the basis of the integration of public datasets from the TCGA and GEO cohorts.

View Article and Find Full Text PDF

Purpose: Investigate the role of lipid metabolism in the tumor immune microenvironment (TIME) of lung adenocarcinoma (LUAD) and identify vital lipid metabolism-related genes (LMRGs) that contribute to immunotherapy outcomes.

Materials And Methods: 1130 LUAD patients were acquired utilizing public databases. Multiple algorithms were used to analyze the contribution of lipid metabolism in TIME.

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!