Purpose <p>Esophageal squamous cell carcinoma (ESCC) is a highly aggressive gastrointestinal malignancy. This study aims to investigate the role and molecular mechanism of a novel circular RNA, circ_0001741, in ESCC progression.</p> Methods <p>The circular structure of circ_0001741 was confirmed by RNase R and actinomycin D assays alongside divergent primer-based amplification targeting its backsplice junction (BSJ). Its expression was profiled using an ESCC tissue microarray. Functional effects of circ_0001741 on proliferation and invasion were assessed using CCK-8 and Transwell assays. The interactions within the circ_0001741/miR-194-5p/E2F3 axis were validated through dual-luciferase reporter, RNA pull-down, and rescue experiments.</p> Results <p>Circ_0001741 was significantly upregulated in ESCC tissues with a 7.5-fold increase compared to adjacent normal tissues. Functional assays demonstrated that silencing circ_0001741 markedly inhibited ESCC cell proliferation and invasion significantly. Mechanistically, circ_0001741 directly sponged miR-194-5p, leading to the upregulation of its target oncogene E2F3. Crucially, the anti-tumor effects induced by circ_0001741 knockdown were significantly reversed by co-silencing miR-194-5p or overexpressing E2F3, thus establishing a functional circ_0001741/miR-194-5p/E2F3 axis in ESCC.</p> Conclusion <p>Our findings establish that circ_0001741 drives ESCC progression by modulating the miR-194-5p/E2F3 axis, underscoring its therapeutic potential for ESCC treatment.</p>

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Circ_0001741 regulates proliferation and invasion in ESCC via the miR-194-5p/E2F3 axis

  • Yuanyuan Wang,
  • Qianqian Sun,
  • Zhuyao Li

摘要

Purpose

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive gastrointestinal malignancy. This study aims to investigate the role and molecular mechanism of a novel circular RNA, circ_0001741, in ESCC progression.

Methods

The circular structure of circ_0001741 was confirmed by RNase R and actinomycin D assays alongside divergent primer-based amplification targeting its backsplice junction (BSJ). Its expression was profiled using an ESCC tissue microarray. Functional effects of circ_0001741 on proliferation and invasion were assessed using CCK-8 and Transwell assays. The interactions within the circ_0001741/miR-194-5p/E2F3 axis were validated through dual-luciferase reporter, RNA pull-down, and rescue experiments.

Results

Circ_0001741 was significantly upregulated in ESCC tissues with a 7.5-fold increase compared to adjacent normal tissues. Functional assays demonstrated that silencing circ_0001741 markedly inhibited ESCC cell proliferation and invasion significantly. Mechanistically, circ_0001741 directly sponged miR-194-5p, leading to the upregulation of its target oncogene E2F3. Crucially, the anti-tumor effects induced by circ_0001741 knockdown were significantly reversed by co-silencing miR-194-5p or overexpressing E2F3, thus establishing a functional circ_0001741/miR-194-5p/E2F3 axis in ESCC.

Conclusion

Our findings establish that circ_0001741 drives ESCC progression by modulating the miR-194-5p/E2F3 axis, underscoring its therapeutic potential for ESCC treatment.