We demonstrated that (i) SLC26A9 expression was significantly upregulated in CRC and correlated with poor prognosis in clinical samples; (ii) SLC26A9 overexpression promotes proliferation and migration, leading to malignant transformation of CRC cells; and (iii) SLC26A9 may interact with β-catenin to participate in the activation of the Wnt/β-catenin signaling pathway and initiate the transcription of downstream target genes. The gene discussed is SLC26A9; the disease is colorectal carcinoma.