Fig 2: Blockade of OLR1/c-MYC/SULT2B1 axis reduces glycolytic metabolism to restrain proliferation and chemoresistance of colon cancer cells.Colon cancer cells were transfected with sh-NC + oe-NC, sh-OLR1 + oe-NC, or sh-OLR1 + oe-SULT2B1. A The mRNA expression of OLR1, c-MYC, and SULT2B1 in colon cancer cells checked by RT-qPCR. B ECAR of colon cancer cells. C Glucose content in colon cancer cells. D Lactate production in colon cancer cells. E The ATP/ADP in colon cancer cells. F RT-qPCR to detect the mRNA expression of GLUT1 and LDHA in colon cancer cells. G The proliferation level of colon cancer cells estimated using MTS. H Detection of colon cancer cell clone formation. I The mRNA expression of Ki67 detected by RT-qPCR. Colon cancer cells were transfected with sh-NC + oe-NC, sh-OLR1 + oe-NC, or sh-OLR1 + oe-SULT2B1, followed by treatment with DDP, oxaliplatin, 5-Fu, and paclitaxel. J The drug resistance of colon cancer cells to DDP, oxaliplatin, 5-Fu, and paclitaxel assessed by MTS. K The expression of P-gp and SMAD4 in colon cancer cells tested by RT-qPCR. The cell experiment was repeated three times. *p < 0.05 between two groups.

Fig 3: The inactivation of OLR1/c-MYC/SULT2B1 axis restrains tumorigenicity and chemoresistance of colon cancer cells in nude mice.A The protein expression of LOX-1, c-MYC, and SULT2B1 detected by western blot analysis. B Growth curve of subcutaneous colon cancer xenograft in nude mice. C Weight of tumor in nude mice. D The expression of Ki67 in tumor tissues of nude mice detected by immunohistochemistry (n = 10 mice/group). *p < 0.05.

Fig 4: Inactivation of c-MYC/SULT2B1 axis disturbs glycolytic metabolism to diminish proliferation and chemoresistance of colon cancer cells.Colon cancer cells were treated with sh-NC + oe-NC, sh-c-MYC + oe-NC, or sh-c-MYC + oe-SULT2B1. A The mRNA expression of c-MYC and SULT2B1 in colon cancer cells tested by RT-qPCR. B Detection of ECAR in colon cancer cells. C Glucose content in colon cancer cells. D Lactate production in colon cancer cells. E The ATP/ADP in colon cancer cells. F RT-qPCR to measure the mRNA expression of GLUT1 and LDHA in colon cancer cells. G MTS to calculate the proliferation level of colon cancer cells. H Colony formation assay to check the level of colony formation in colon cancer cells. I Detection of Ki67 mRNA expression in colon cancer cells by RT-qPCR. Colon cancer cells were treated with sh-NC + oe-NC, sh-c-MYC + oe-NC, or sh-c-MYC + oe-SULT2B1, followed by treatment with DDP, oxaliplatin, 5-Fu, and paclitaxel. J The drug resistance of colon cancer cells to DDP, oxaliplatin, 5-Fu, and paclitaxel detected by MTS. K RT-qPCR for detecting the mRNA expression of P-gp and SMAD4 in colon cancer cells. The cell experiments were repeated three times. *p < 0.05 between two groups.

Fig 5: c-MYC knockdown diminishes SULT2B1 expression and dampened glycolytic metabolism of colon cancer cells.A The downstream genes of transcription factor c-MYC predicted by hTFtarget and intersected with 45 obviously upregulated genes to obtain 12 genes. B Clinical data of TCGA analyzed by GEPIA to draw the survival curve between SULT2B1 expression and colon cancer. C The protein expression of c-MYC in colon cancer and adjacent normal tissues detected by immunohistochemistry (adjacent tissues: n = 120; tumor tissues: n = 120; ×200). D The mRNA expression of c-MYC and SULT2B1 in colon cancer cells after overexpression and knocking down c-MYC determined by RT-qPCR. E Detection of ECAR in colon cancer cells after knocking down c-MYC. F Detection of glucose content in colon cancer cells after knocking down c-MYC. G Detection of lactate production in colon cancer cells after knocking down c-MYC. H Detection of ATP/ADP in colon cancer cells after knocking down c-MYC. I RT-qPCR to detect the mRNA expression of GLUT1 and LDHA in colon cancer cells after knocking down c-MYC. The cell experiment was repeated three times. *p < 0.05 between two groups.