<b>Conclusion:</b> Based on these data, we demonstrated that FENDRR may function as a tumor-suppressor gene by repressing SOX4 and as a potential therapeutic target for colon cancer.
<b>Conclusions:</b> These results indicate that G9a-induced and p53-dependent epigenetic programing stimulates the growth of colon cancer, which also suggests that G9a inhibitors that restore p53 activity are promising therapeutic agents for treating colon cancer, especially for CRC expressing wild-type p53.
<b>Methods:</b> In this study we investigated colon cancer cell sphere and its differential expression of PRMT8 compared with colon cancer cells grown by static adherence.
<b>Methods:</b> Patient-derived tumor cells were collected from the ascites of a refractory colon cancer patient with wild-type RAS and PIK3CA mutation.
<b>SLN</b> can not only mark the Dvl protein in the Wnt pathway to recognize tumors layer by layer but also achieve effective inhibition of colon cancer, providing a promising reagent for chemotherapy and a fluorescent indicator for surgery during the removal the colon tumors in situ.
<b>SLN</b> can not only mark the Dvl protein in the Wnt pathway to recognize tumors layer by layer but also achieve effective inhibition of colon cancer, providing a promising reagent for chemotherapy and a fluorescent indicator for surgery during the removal the colon tumors in situ.
<i>AC</i> can be a potent synergistic adjuvant, down-regulates cancer stemness genes and enhances the antitumor ability of 5-FU by stimulating apoptosis-associated genes, suppressing inflammation and metastasis genes through miR142-3p in colon cancer.