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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Lnc-RP11-536 K7.3/SOX2/HIF-1α signaling axis regulates oxaliplatin resistance in patient-derived colorectal cancer organoids

Fig. 3

Knockout of lnc-RP11-536 K7.3 attenuated glycolysis and angiogenesis. A-H Determination of glucose uptake (A and E), ATP (B and F), NADPH (C and G), and lactate production (D and H) in CC organoids and cells as described in Methods. Data were presented as mean ± SD of triplicate measurements repeated three times with similar results. Statistical significance was assessed via the Student’s t-test(**P < 0.01). I-J Measurement of ECAR (I) and OCR (J) in CC organoids and cells as described in Methods. K Cell viability assay of organoids treated with 1 uM oxaliplatin alone or in combination with 2.5 mM 2-DG in different time intervals. L IC50 values of cisplatin. CC cells were treated with different concentrations of oxaliplatin with or without 2-DG (5 mM for 48 h) (**P < 0.01). M Colony formation efficiency of chemo-resistant CC organoids and cells treated with 2 uM oxaliplatin alone or in combination with 2.5 mM 2-DG for 7 days (**P < 0.01). N-O Effects of knockout of lnc-RP11-536 K7.3 on HUVECs. HUVECs were treated with supernatant obtained from CR-RKO/KO1-RP11-536 K7.3, CR-RKO/KO2-RP11-536 K7.3 or the corresponding control cells. Represent pictures of different groups (N). Statistical analysis of tube formation and relative colony formation effciency (**P < 0.01) (O). Above experiments were repeated 3 times

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