The purpose of the paper was to explore the regulation relationship between hypoxia and BCL9 in colorectal cancer cells and whether the BCL9 can influence the function of colorectal cancer cells.

Detected BCL9 in 20 cases of colorectal cancer and the normal colorectal tissue by immunohistochemistry and RT-qPCR; Assay the BCL9 expression in colorectal cancer cells under hypoxia condition or normoxia condition by RT-PCR and western-blot; Constructed luciferase plasmid which contain of the promoter of BCL9, by given the hypoxia condition to induce endogenous HIF-1α or use over-expression plasmid induced exogenous HIF-1α in HCT116 cells to explored the regulate relationship between HIF-1α and LDHA; Middle the expression of BCL9 by over-expression plasmid and siRNA, and detected the proliferation and migration by CCK8 assay and transwell assay.

BCL9 is always over-expression in colorectal cancer [(3.25±0.53) vs. (1.03±0.12), P<0.05]; By given oxygen condition, we found that hypoxia can induce BCL9 over-expression in colorectal cancer cells [(6.71±0.83) vs.(1.54±0.21), P<0.05]; Both hypoxia and over-expression exogenous HIF-1α leaded luciferase activity enhanced; Using RNA interfere technique to knockdown the expression of HIF-1α will suppression LDHA expression [(3.53±0.75) vs. (0.96±0.15), (4.83±0.62) vs. (1.02±0.14); P<0.05]; Interfere the expression of BCL9 suppresion HCT116 cells proliferation and migration [(1.23±0.12) vs. (1.87±0.15), P<0.05]; On the other hand, over-expression BCL9 leaded to the opposite result [(2.43±0.16) vs. (1.81±0.14), P<0.05];

Hypoxia induce BCL9 over-expression and promote HCT116 cells proliferation and migration.