# HEY1 promotes the development and metastasis of osteosarcoma through CD44/EGFR/FAK pathway

## TL;DR

This study identifies HEY1 as a key gene that promotes osteosarcoma growth and spread through a specific signaling pathway.

## Contribution

The novel contribution is the discovery of HEY1's role in osteosarcoma via the CD44/EGFR/FAK pathway.

## Key findings

- HEY1 is significantly overexpressed in osteosarcoma tissues and cells.
- HEY1 knockdown inhibits osteosarcoma cell proliferation.
- HEY1 interacts with CD44 and influences the EGFR-FAK pathway.

## Abstract

Osteosarcoma (OS) is a highly prevalent and deadly malignant tumour primarily affecting adolescents. However, the identification of new therapeutic targets remains an urgent need. The advent of bioinformatics technology has offered us a novel approach to screen key genes from diverse OS‐related databases, thereby providing valuable insights into the mechanistic understanding of OS prognosis. In this study, we comprehensively integrated multiple databases to identify the crucial oncogene, HEY1, which exerts a significant impact on OS prognosis. Subsequently, we conducted a experimental validations to explore influence of HEY1 knockdown on OS cells. HEY1 exhibited significant overexpression in OS tissues and cells and its silencing resulted in a significant inhibition of proliferation. The interaction between HEY1 and CD44 was identified through transcriptome sequencing and mass spectrometry analysis. Additionally, our findings suggested that HEY1 could potentially influence the EGFR‐FAK pathway. Further experiments established that HEY1 regulates the EGFR‐FAK pathway via CD44, thereby influencing the biological phenotype of OS cells. These findings were subsequently validated using in vivo animal models. In summary, HEY1 demonstrated significant overexpression in both OS tissues and cells, exerting a substantial impact on the prognosis of OS.