Lactylation of SLC26A3 in the acidic tumor microenvironment promotes malignant progression of colorectal carcinoma

This work investigates how the acidic tumor microenvironment drives colorectal cancer progression through protein lactylation. The authors show that lactylation decreases SLC26A3 stability and expression, weakens its interaction with HuR/CUGBP1, and promotes oncogenic mRNA regulation associated with recurrence, metastasis, and drug resistance. These findings position SLC26A3-related pathways as promising therapeutic and prognostic targets in colorectal carcinoma.