Abstract

Objective We investigated how circ-0058514 modulates esophageal carcinoma cell behavior through its regulation of the miR-301b/COL1A1 signaling axis. Methods Eca109 cells were allocated into six experimental cohorts: si-0058514 transfection, si-NC control, miR-301b overexpression, miR-NC control, combined si-0058514 with anti-miR-301b treatment, and untreated control. Expression profiling of circ-0058514 and miR-301b was performed via RT-PCR in both Eca109 esophageal carcinoma cells and HET-1A immortalized normal esophageal epithelial cells. Cellular proliferation was assessed using CCK-8 assays, while Transwell chambers evaluated invasive capacity. Flow cytometry quantified apoptotic rates, and Western blotting determined COL1A1 protein abundance. Dual-luciferase reporter assays validated the targeting relationship between circ-0058514 and the miR-301b/COL1A1 axis. Results Expression analysis revealed significant miR-301b downregulation in Eca-109 malignant cells compared to HET-1A normal epithelium, while circ-0058514 exhibited inverse expression patterns with marked upregulation in cancer cells (P < 0.0001). Knockdown of circ-0058514 significantly impaired malignant phenotypes, including reduced viability, diminished invasive capacity, and decreased COL1A1 protein levels, while concurrently enhancing apoptotic susceptibility compared to si-NC controls (P < 0.0001). Conversely, miR-301b overexpression produced similar anti-tumor effects, with reduced proliferation, invasion, and COL1A1 expression, alongside increased apoptosis relative to miR-NC controls (P < 0.0001). Luciferase assays confirmed that wild-type circ-0058514/COL1A1 constructs significantly suppressed miR-301b activity compared to miR-301b-NC group (P < 0.0001). Rescue experiments demonstrated that combined si-0058514 and anti-miR-301b treatment yielded higher proliferation, invasion, and COL1A1 expres