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The objectives of this study were to investigate the expression of MSX1 in cervical cells and tissues, the methylation status of the MSX1 promoter, the influence of overexpression of gene MSX1 on the proliferation, migration, and invasion of HeLa and SiHa cells, and finally the possible molecular mechanisms responsible for the suppressive effects of MSX1 upon cervical cancer cells.

<em>MSX1</em> induces G0/G1 arrest and apoptosis by suppressing Notch signaling and is frequently methylated in cervical cancer