In many cancers, chemotherapy resistance is thought to result from slowly cycling cells with stem cell-like characteristics, which may be caused by epigenetic plasticity. Previous reports have characterized the biology associated with chemotherapy-resistant cells, but the molecular pathways by which such cells are generated from cycling cancer populations have not been fully identified. We have previously shown that colorectal cancer stem cell-like cells (CSCs) can be classified into several groups and that PROX1-positive slow-cycling CSCs contribute to chemotherapy resistance. Therefore, we performed PROX1 ChIP-seq analysis in stem cell-like cells of colorectal cancer to analyze the molecular mechanism by which PROX1 maintains chemoresistance.