The results of mechanistic experiments illustrated that CAFs delivered UCA1 to CRC cells and promoted the upregulation of mTOR, while the UCA1/mTOR regulatory axis inhibited the expression of p27 and miR-143 and promoted the expression of Cyclin-D1 and Kirsten rat sarcoma (KRAS) thus promoting the malignant progression of CRC (118) miR-224-5p expression was significantly increased in CRC and targeted to suppress SLC4A4 expression. The gene discussed is UCA1; the disease is colorectal carcinoma.