Scholarlink

Background <p>Esophageal cancer (EC) is still a difficult problem in medicine, depriving many patients of their lives every year. RAD18 and ATM were implicated in cancers including esophageal squamous cell carcinoma (ESCC). However, whether RAD18/ATM axis influences ESCC progression remains unclear.</p> Methods <p>The abundance of genes and proteins was evaluated using RT-qPCR and western blot. Cell proliferation, migration and invasion were examined using clone formation, scratch test and transwell. The level of ATM ubiquitination was verified and experimented using Co-IP.</p> Results <p>Our findings found that RAD18 expression was enhanced in TCGA database, in ESCC patients and ESCC cells. Similarly, ATM expression was declined in ESCC patients and ESCC cells. RAD18 silencing resulted in suppression of cell proliferation, migration and invasion of ESCC cells, which were abolished by ATM silencing. In addition, ATM silencing promoted malignant behaviors of ESCC cells by activating STAT3/PD-L1 axis, which was reversed by PD-L1 knockdown. Moreover, RAD18 could reduce ATM protein levels.</p> Conclusion <p>RAD18 mediated ATM ubiquitination to reduce ATM protein level, thereby activating STAT3/PD-L1 axis and strengthening cell proliferation, migration and invasion of ESCC cells.</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

RAD18 promotes cell malignant behaviors of esophageal squamous cell carcinoma by modulating ATM/STAT3/PD-L1

  • 期刊论文

  • 发表日期：

    2025年7月9日

查看全文
  • Xianghui Yang,
  • Qishi Song,
  • Min Li,
  • Da Liu

摘要

Background

Esophageal cancer (EC) is still a difficult problem in medicine, depriving many patients of their lives every year. RAD18 and ATM were implicated in cancers including esophageal squamous cell carcinoma (ESCC). However, whether RAD18/ATM axis influences ESCC progression remains unclear.

Methods

The abundance of genes and proteins was evaluated using RT-qPCR and western blot. Cell proliferation, migration and invasion were examined using clone formation, scratch test and transwell. The level of ATM ubiquitination was verified and experimented using Co-IP.

Results

Our findings found that RAD18 expression was enhanced in TCGA database, in ESCC patients and ESCC cells. Similarly, ATM expression was declined in ESCC patients and ESCC cells. RAD18 silencing resulted in suppression of cell proliferation, migration and invasion of ESCC cells, which were abolished by ATM silencing. In addition, ATM silencing promoted malignant behaviors of ESCC cells by activating STAT3/PD-L1 axis, which was reversed by PD-L1 knockdown. Moreover, RAD18 could reduce ATM protein levels.

Conclusion

RAD18 mediated ATM ubiquitination to reduce ATM protein level, thereby activating STAT3/PD-L1 axis and strengthening cell proliferation, migration and invasion of ESCC cells.