Fig. 3.

METTL17 deficiency reduces xenograft tumor growth and AOM/DSS-induced CRC tumorigenesis in vivo.

A, B and C. Knockdown of METTL17 inhibited SW620 xenograft tumor growth (A) and reduced tumor size (B) and weights (C) in mice. n = 6 per group.

D and E. Knockdown of METTL17 led to a reduction in the protein expression of β-Catenin and c-Myc, while the PCNA protein level remained unchanged, as analyzed by Western blot (D). The relative expression was quantified by normalizing to β-actin (E). n = 4 per group.

F. Knockdown of METTL17 caused reduced β-Catenin expression, but unchanged Ki-67 positive cells in SW620 xenograft tumors. H&E, β-Catenin, and Ki-67 staining were performed on tissue sections from Scramble and METTL17 knockdown SW620 tumors (Scale bar = 100 μm). The β-Catenin signal and Ki-67-positive tumor cells were quantified in the 400 × field, n = 4 per group.

G and H.Mettl17 heterozygote mice (Mettl17^+/−) showed a decreased incidence of AOM/DSS-induced CRC formation compared to WT mice. Representative images of intact tumors were shown (G). Mettl17^+/− mice exhibited fewer and smaller colon tumors after AOM/DSS treatment, as indicated by the number of total tumors per colon (up) and different sizes' tumors per colon (down) (H). n = 12 per group.

I and J. Colon tumors in Mettl17^+/− mice exhibited reduced levels of PCNA and β-Catenin proteins, with no significant change observed in c-Myc, as analyzed by Western blot (I). The relative expression was respectively quantified by normalizing to β-actin (J). n = 4 per group.

K. H&E, Ki-67, and β-Catenin staining were performed on colon sections from WT and Mettl17^+/− mice after AOM/DSS treatment.

Data are shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, based on two-sided Student's t-test.