Fig. 7
Targeting browning or FFAs uptake enhances the anti-tumor efficacy of oxaliplatin in vivo. a Flowchart of constructing the subcutaneous tumor-bearing model and implementing combined therapy in C57B/L6 mice, using oxaliplatin (5 mg/kg), SR59230A (8 mg/kg), and SSO (20 mg/kg) through intraperitoneal injection (i.p.). b–d Subcutaneous tumor growth curve b of CMT93 scramble or stable Miip knockdown cells (1 × 105 cells per mouse) mixed with 3T3-L1 cells (2.5 × 104 cells per mouse). Treatment (vehicle, oxaliplatin, oxaliplatin plus SR59230A or SSO) began when the volume of allografts reached approximately 150 mm3. The allograft tumors were removed (c, scale bar: 1 cm) and weighed d at the end of the experiment (n = 5). e–f Kaplan–Meier analysis of disease-free survival for gene signatures related to adipocyte browning (AZGP1/UCP1/PPARGC1A, e and FFAs transportation and oxidation (CD36/FABP4/CPT1A, f) in COAD and READ patients. g The graphical abstract describes how abnormal MIIP expression leads to excessive secretion of AZGP1, promoting bi-directional communication between CRCs and surrounding adipose tissue, and the consequent tumor-supportive role of FFAs released from adjacent adipocytes in the TME. All data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001