Illustration of LINRIS-IGF2BP2-MYC axis in CRC. a Representative IHC images of Ki-67, IGF2BP2, MYC, GLUT-1 and PKM2 and LDHA in tumor tissues from patients with CRC (n = 220) with low or high levels of LINRIS. Scale bar, 50 μm. b Percentages of specimens showing different levels of Ki-67, IGF2BP2, MYC, GLUT-1 and PKM2 and LDHA in the low or high LINRIS expression groups (n = 220, Chi-square test, **P < 0.01). c and d Representative IHC images (c) and statistical analysis (d) of IGF2BP2 expression in CRC and matched normal tissues. The data are shown as the mean ± SD; n = 220, two-tailed Student’s t-test. e Kaplan-Meier analysis of the OS curves for CRC patients with low (n = 118) or high (n = 102) IGF2BP2 expression (log-rank test). f Kaplan-Meier analysis of the OS curves for CRC patients with LINRIS/IGF2BP2-high (both levels of LINRIS and IGF2BP2 were high, n = 76), LINRIS/IGF2BP2-low (both levels of LINRIS and IGF2BP2 were low, n = 76) or intermediate (n = 68) expression (log-rank test). g Proposed working model of this study. LINRIS stabilized IGF2BP2 by binding to its K139 ubiquitination site and subsequently maintained the MYC-induced glycolysis and proliferation of CRC cells. Otherwise, inhibition of LINRIS, such as by GATA3, resulted in more degradation of IGF2BP2 through the ubiquitination-autophagy pathway.