MLL
protein genes encode a family of crucial
transcription factors that play a key role in multiple
cancer development. The functions of different MLL
proteins have not been definitively studied. MLL1 is a
histone methyltransferase that mediates
histone H3 lysine 4, and it has been found to have aberrant expression in several
tumors. However, the function of MLL1 in cervical
carcinoma is little known. We used tissue analysis, cell culture experiments, and molecular profiling to investigate the mechanism of MLL1 in cervical
carcinoma development. We report here that MLL1 is overexpressed in cervical
carcinoma tissues and cell lines, and its overexpression is correlated with the
tumor grade. Through FACScan flow cytometry assay, we found that MLL1 promotes cell proliferation by promoting the G1/S transition through transcriptional activation of CCND1 in cervical
carcinoma cells. Furthermore, we utilized co-immunoprecipitation and
glutathione S-transferase pull-down assays to identify β-
catenin as the transcription partner for MLL1 and demonstrated that MLL1 and β-
catenin act in synergy in the transcriptional activation of CCND1 in cervical
carcinoma cells. In addition, transwell assay and anchorage-independent cell growth assay also revealed that MLL1 promotes
metastasis of cervical
carcinoma cells through interaction with β-
catenin. Our study not only demonstrated a role for MLL1 in the proliferation and
metastasis of cervical
carcinoma cells but also revealed the interaction of MLL1 with β-
catenin to play a different role.