敲减CMTM3增加急性B淋巴细胞白血病细胞对伊马替尼敏感性
A, SUP-B15 and BV173 cells were infected with CMTM3 shRNA (sh391, sh393) or the matching control non-targeting shRNA (shN), and Western blot analysis of Ph+B-ALL cell lines to detect the expression of BCR-ABL; B, Erk and Akt levels treated with imatinib for 24 h were analyzed by Western blot; C, go enrichment analysis (shN/sh391) (1, L-alpha-amino acid transmembrane transport; 2, regulation of non-canonical Wnt signaling pathway; 3, regulation of double-strand break repair via nonhomologous end joining; 4, amino acid transmembrane transport; 5, tau-protein kinase activity; 6, cellular response to oxygen-containing compound; 7, cleavage in ITS2 between 5.8S rRNA and LSU-rRNA of tricistronic rRNA transcript; 8, positive regulation of double-strand break repair via nonhomologous end joining; 9, positive regulation of non-canonical Wnt signaling pathway; 10, negative regulation of collateral sprouting); D, knockdown of CMTM3 regulates some molecules by mass spectrometry analysis. Erk, extracellular signal-regulated kinase; Akt, protein kinase B; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; RNF213, E3 ubiquitin ligase ring finger protein 213; FERMT1, fermitin family member 1; AES, amino-terminal enhancer of split; ZEB2, zinc finger E-box binding homeobox 2; RhoGTP4, Rho guanosine triphosphate 4; CK1δ, casein kinase 1δ; FAM53B, family with sequence similarity 53, member B. Data (A to B) were representative of three independent experiments. One-way ANOVA and two-way ANOVA with Dunnett's multiple comparisons test and presented as the ˉx±s (*P < 0.05, # P < 0.01, ★P < 0.001).
