本研究的目的是探究circ-POLA2在结肠癌（CC）中的机制。记录了CC组织和细胞中circ-POLA2、miR-138-5p和SEMA4C的水平。确定了circ-POLA2、miR-138-5p或SEMA4C对细胞增殖、迁移、侵袭和凋亡的影响。调查了circ-POLA2/miR-138-5p/SEMA4C的反馈环路。经测量，circ-POLA2和SEMA4C的表达水平较高，而miR-138-5p的表达水平较低。同时，circ-POLA2通过miR-138-5p靶向调控SEMA4C的表达。circ-POLA2的敲除导致细胞活动的阻断，但这一效应可以通过抑制miR-138-5p或过表达SEMA4C来缓解。总体而言，circ-POLA2通过miR-138-5p/SEMA4C轴对CC具有致瘤作用，这可能为CC治疗提供了有希望的分子靶点。

This study aimed to investigate the mechanism of circ-POLA2 in colon cancer (CC). Circ-POLA2, miR-138-5p, and SEMA4C levels in CC tissues and cells were recorded. The influences mediated by circ-POLA2, miR-138-5p or SEMA4C on cell proliferation, migration, invasion, and apoptosis were determined. The feedback loop of circ-POLA2/miR-138-5p/SEMA4C was surveyed. As measured, circ-POLA2 and SEMA4C were highly expressed, while miR-138-5p was poorly expressed. Meanwhile, circ-POLA2 could mediate SEMA4C through miR-138-5p targeting. Circ-POLA2 knockdown caused the blockade for cell activities, but this effect was alleviated by miR-138-5p inhibition or SEMA4C overexpression. Overall, circ-POLA2 is tumorigenic for CC through miR-138-5p/SEMA4C axis, which may provide a promising molecular target for CC therapy.