Fig. 4: METTL3 deletion reduces AML chemosensitivity by inducing adipogenic differentiation of OP9 cells.

A Representative images and quantification of ORO staining in Mettl3 overexpression cells after 14 days of adipogenic induction. Scale bar, 100 µm. B qPCR analysis of the expression of adipogenic marker genes, Adipoq, Cebpa, Lpl, Plin1, CD36, and Pparγ in Mettl3 overexpression cells under adipogenic conditions. C ORO staining of Mettl3 knockdown cells following adipogenic induction. Scale bar, 100 µm. Absorbance at OD₅₀₀ was determined for ORO staining in isopropanol at room temperature. D qPCR analysis of adipogenic lineage–associated gene expression after induction of differentiation in Mettl3 knockdown cells. E ELISA detection of adipokine concentration in the culture medium before induction of differentiation and on day 14 of Mettl3 overexpression cells. F ELISA detection of adipokine concentration in the culture medium before induction of differentiation and on day 14 of Mettl3 knockdown cells. G After adipogenic differentiation of Mettl3 overexpression cells, AML cells were co-cultured with them for 24 h to test their chemoresistance to Ara-C and DNR. H After adipogenic differentiation of Mettl3 knockdown cells, AML cells were co-cultured with them for 24 h to test their chemoresistance to Ara-C and DNR. Blank, blank control; OE-NC, negative control of overexpression; Mettl3-OE, overexpression of mouse Mettl3; sh-NC, negative control of knockdown; shMettl3-1 and shMettl3-2, independent shRNAs targeting mouse Mettl3. The data are presented as mean ± SD. The two-tailed unpaired Student’s t test was used to compare two groups and one-way ANOVA with Dunnett’s multiple comparisons test was performed for multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns not significant.