Scholarlink

Background <p>Osteosarcoma (OS) faces a high metastatic burden, limited effective treatments, and a lack of specific therapeutic targets.</p> Methods <p>In this prospective study, we established a human osteosarcoma cell (HOS) model overexpressing lncRNA FEZF1-AS1 (OE FEZF1-AS1), and subsequently obtained FEZF1-AS1-affected transcriptome data using high-throughput RNA sequencing (RNA-seq).</p> Results <p>OE FEZF1-AS1 promoted HOS cell proliferation and invasion, upregulated 125 genes, suppressed 48 genes, and impacted 1156 alternative splicing events (ASEs), including pathways like C-type lectin receptor signaling and <i>Yersinia pestis</i> infection.</p> Conclusions <p>LncRNA FEZF1-AS1 plays a pivotal role in promoting the proliferation and invasion of HOS cells. Moreover, our study provides a comprehensive gene screening approach for identifying potential targets of FEZF1-AS1, emphasizing their regulatory mechanisms and ASEs in OS.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

LncRNA FEZF1-AS1 regulates the gene expression and alternative splicing associated with osteosarcoma

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月3日

查看全文
  • Yanlong Han,
  • Ziang Ye,
  • Li Wang

摘要

Background

Osteosarcoma (OS) faces a high metastatic burden, limited effective treatments, and a lack of specific therapeutic targets.

Methods

In this prospective study, we established a human osteosarcoma cell (HOS) model overexpressing lncRNA FEZF1-AS1 (OE FEZF1-AS1), and subsequently obtained FEZF1-AS1-affected transcriptome data using high-throughput RNA sequencing (RNA-seq).

Results

OE FEZF1-AS1 promoted HOS cell proliferation and invasion, upregulated 125 genes, suppressed 48 genes, and impacted 1156 alternative splicing events (ASEs), including pathways like C-type lectin receptor signaling and Yersinia pestis infection.

Conclusions

LncRNA FEZF1-AS1 plays a pivotal role in promoting the proliferation and invasion of HOS cells. Moreover, our study provides a comprehensive gene screening approach for identifying potential targets of FEZF1-AS1, emphasizing their regulatory mechanisms and ASEs in OS.