Abstract: Metastasis and tumor stem cell characteristics of colorectal cancer are key factors contributing to poor patient prognosis, yet their molecular regulatory mechanisms remain incompletely elucidated. This study found that miRNA miR-144-3p is significantly underexpressed in colorectal cancer cells, while its potential target gene prostaglandin-endoperoxide synthase 2 (PTGS2) is overexpressed, suggesting that both may be involved in the regulation of malignant progression in colorectal cancer. Using a dual-luciferase reporter gene system, it was confirmed that miR-144-3p can directly target and inhibit PTGS2 expression. In vitro experiments demonstrated that miR-144-3p significantly suppresses the migration and invasion capabilities of colorectal cancer cells, as well as tumor sphere formation efficiency. It also downregulates the expression of the stem cell marker cluster of differentiation 133 (CD133) and core transcription factors Nanog homeobox (Nanog), SRY-box transcription factor 2 (SOX2), and octamer binding transcription factor 4 (OCT4). In vivo, a nude mouse xenograft tumor model further validated that overexpression of miR-144-3p can markedly inhibit tumor growth and reduce PTGS2 expression level. Mechanistically, miR-144-3p weakens tumor cell stemness maintenance and the epithelial-mesenchymal transition (EMT) process by negatively regulating the PTGS2/prostaglandin E2 (PGE2) signaling pathway, thereby exerting an antitumor effect. This study is the first to reveal the inhibitory effect of the miR-144-3p-PTGS2 axis on the regulation of stemness characteristics in colorectal cancer, providing a new theoretical basis and potential therapeutic strategy for targeted intervention in colorectal cancer progression.

Keywords: colorectal cancer; nude mouse xenograft; migration; invasion; cell stemness

（Acta Laser Biology Sinica, 2026, 35(4): 352-360）