Scholarlink

Background <p>Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors, characterized by high recurrence and mortality rates. The inflammatory microenvironment plays a crucial role in cancer initiation and progression. The RSF1 gene, associated with hepatitis, generates circular RNA during transcription, which is intricately linked to liver diseases and inflammatory processes. We sought to explore the role of inflammation-related circRSF1, which may play an important role in the occurrence and development of HCC in vitro.</p> Methods <p>We successfully established an in vitro HCC progression model using IL-1β-treated HepG2 cells. CircRSF1 expression measured was in HCC tissue and IL-1β-treated HepG2 cells by quantitative RT‑PCR. EIF4A3 expression was detected by western blot. Cell proliferation assay was performed by cck-8 assay. Cell migration and invasion was performed by transwell assay. The binding relationship of circRSF1 and EIF4A3 was confirmed by RNA binding protein immunoprecipitation assay and RNA pull down assay. Role of circRSF1 and EIF4A3 in HCC progress in vivo was evaluated nude mouse xenograft model.</p> Results <p>IL-1β upregulated circRSF1 expression in HepG2 cells. Consistently, elevated circRSF1 levels were also observed in clinical HCC samples. Functional studies demonstrated that circRSF1 knockdown suppressed IL-1β-induced proliferation, migration, and invasion of HepG2 cells. Further mechanistic investigations revealed stable binding sites between circRSF1 and EIF4A3. Silencing EIF4A3 enhanced the biodegradation of circRSF1, suggesting that circRSF1 depends on EIF4A3 to maintain its stability. In vivo, knockdown of EIF4A3 reduced the tumor volume and weight, which was reversed by circRSF1 overexpression.</p> Conclusions <p>Our findings indicate that circRSF1, stabilized by EIF4A3, promotes the malignant progression of HepG2 cells in vitro. These results suggest that circRSF1 may function as an oncogene in inflammation-mediated HCC progression, highlighting its potential as a therapeutic target.</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

CircRSF1 Promoted HepG2 Cell Proliferation, Migration and Invasion Depending on EIF4A3

  • 期刊论文

  • 发表日期：

    2026年3月17日

查看全文
  • Dan Huang,
  • Zhonghui Zhu

摘要

Background

Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors, characterized by high recurrence and mortality rates. The inflammatory microenvironment plays a crucial role in cancer initiation and progression. The RSF1 gene, associated with hepatitis, generates circular RNA during transcription, which is intricately linked to liver diseases and inflammatory processes. We sought to explore the role of inflammation-related circRSF1, which may play an important role in the occurrence and development of HCC in vitro.

Methods

We successfully established an in vitro HCC progression model using IL-1β-treated HepG2 cells. CircRSF1 expression measured was in HCC tissue and IL-1β-treated HepG2 cells by quantitative RT‑PCR. EIF4A3 expression was detected by western blot. Cell proliferation assay was performed by cck-8 assay. Cell migration and invasion was performed by transwell assay. The binding relationship of circRSF1 and EIF4A3 was confirmed by RNA binding protein immunoprecipitation assay and RNA pull down assay. Role of circRSF1 and EIF4A3 in HCC progress in vivo was evaluated nude mouse xenograft model.

Results

IL-1β upregulated circRSF1 expression in HepG2 cells. Consistently, elevated circRSF1 levels were also observed in clinical HCC samples. Functional studies demonstrated that circRSF1 knockdown suppressed IL-1β-induced proliferation, migration, and invasion of HepG2 cells. Further mechanistic investigations revealed stable binding sites between circRSF1 and EIF4A3. Silencing EIF4A3 enhanced the biodegradation of circRSF1, suggesting that circRSF1 depends on EIF4A3 to maintain its stability. In vivo, knockdown of EIF4A3 reduced the tumor volume and weight, which was reversed by circRSF1 overexpression.

Conclusions

Our findings indicate that circRSF1, stabilized by EIF4A3, promotes the malignant progression of HepG2 cells in vitro. These results suggest that circRSF1 may function as an oncogene in inflammation-mediated HCC progression, highlighting its potential as a therapeutic target.