Research Paper Volume 12, Issue 1 pp 156—177

Over-expression of EGFR regulated by RARA contributes to 5-FU resistance in colon cancer

Figure 5. EGFR contributes to 5-FU resistance in colon cancer cells through autophagy. (A) Autophagy induction was increased in HT29-R cells compared with parental HT29 cells (n=3). (B) Conversion of LC3-I to LC3-II was increased in HT29-R cells compared with parental HT29 cells (n=3, *P < 0.05 versus control). (C) Knockdown of EGFR in HT29-R cells impaired autophagy flux (n=3). (D) Knockdown of EGFR in HT29-R cells inhibited the conversion of LC3-I to LC3-II (n=3, *P < 0.05 versus control). (E) Fluorescence images of mRFP-GFP-LC3 in HT29-R cells transfected with control siRNA or EGFR siRNA (200× magnification). (F) Rapamycin reversed autophagy inhibition induced by EGFR knockdown in HT29-R cells (n=3). (G) Rapamycin reversed the inhibition of LC3-I to LC3-II conversion caused by EGFR knockdown (n=3, *P < 0.05 versus control). (H) Rapamycin restored 5-FU resistance in HT29-R cells transfected with EGFR siRNA (n=3).