Colorectal cancer is one of the most common malignancies and the leading cause of cancer-related death in worldwide. The objective of current research was to analyze the role of β-cateinin in the colorectal cancer progression. The cell phenotype was measured by CCK-8, Colony formation and transwell assays. RT-qPCR and western blot was carried out to test the RNA levels. Beisdes, the β-cateinin and were confirmed by immunofluorescence. The lactylation levels were analyzed using pan-kla antibody. Cycloheximide was used to assessed the stability of β-cateinin protein. The results showed that β-cateinin was up-regulated in colorectal cancer tissues and colorectal cancer cells under hypoxia treatment. β-cateinin silencing prevented the cell growth and promoteed the apoptosis of colorectal cancer cells. Besides, hypoxia treatment aggravated cell growth and metastasis, which was neutralized by β-cateinin knockdown. Additionally,  β-cateinin was confirmed to be modified by lactylation, which then promoted the protein stability of it. Furthermore, β-cateinin knockdown declined the c-myc levels, while promoted that of APC. In conclusion, hypoxia promoted lactylation and protein stability of β-cateinin. β-cateinin mediates  the malignant behaviors of colorectal cancer cells under hypoxia condition through elevating the c-myc and APC levels.

β-cateinin lactylation promoted the colorectal cancer progression through wnt signaling pathway

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