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Fig. 3 | Clinical Epigenetics

Fig. 3

From: Investigating the mechanisms by which low NAT1 expression in tumor cells contributes to chemo-resistance in colorectal cancer

Fig. 3

Silencing NAT1 enhances chemo-resistance in CRC by promoting LGR5+ CSC formation. A Flow cytometry was used to quantify the proportions of CD44+, CD133+, CD166+, and LGR5+ cell subpopulations in CaCO2 cells treated with 1.68 μmol docetaxel or DMSO for 48 h. B CaCO2 cells were treated with 8.52 μmol vinblastine, 1.68 μmol docetaxel, 5.49 μmol gemcitabine, 10.94 μmol vincristine, and 11.71 μmol daporinad or DMSO for 48 h. HCT116 cells were treated with 4.87 μmol vinblastine, 1.68 μmol docetaxel, 5.49 μmol gemcitabine, 10.94 μmol vincristine, and 11.71 μmol daporinad or DMSO for 48 h. Flow cytometry was used to quantify the proportion of LGR5+ subpopulation in CaCO2 and HCT116 cells. C Compared to their respective control groups, the proportion of LGR5+ cells was significantly increased in the sh-NAT1 group, whereas it was significantly decreased in the OE-NAT1 group. Statistical significance is denoted as ns represents no significance, *P < 0.05. Comparison of sh-NC with sh-NAT1 and OE-NC with OE-NAT1 via unpaired t-test. The experiments were independently repeated at least three times

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