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Fig. 7 | Molecular Cancer

Fig. 7

From: 3-BrPA eliminates human bladder cancer cells with highly oncogenic signatures via engagement of specific death programs and perturbation of multiple signaling and metabolic determinants

Fig. 7

Critical regulators of glucose homeostasis are detrimentally targeted after bladder cancer cell exposure to 3-BrPA: drug-induced splicing silencing of GLUT4 RNA. (a-b) Representative (three independent experiments) Western blotting profiles of whole-cell protein extracts obtained from RT4, T24 and T24-X cells, seeded at ~60 % confluency and exposed to the indicated doses of 3-BrPA for 24 h. The proteins examined were HK2, GAPDH, p-AS160-Thr642, AS160, Rab10, Tug (a), GLUT1 and GLUT4 (b), while Actin was used as molecule of reference. (c-f) Gene expression profiles, as evidenced through employment of RT-sqPCR protocols (three independent experiments), using total RNA preparations derived from RT4, T24 and T24-X cells, grown at ~60 % confluency and treated with the indicated doses of 3-BrPA (c-f), Taxol and Doxorubicin (f) for 24 h (also, see Additional file 5: Figure S5, Additional file 6: Figure S6 and Additional file 7: Figure S7). Besides the oligonucleotide primers able to specifically recognize the GLUT1, GLUT2, GLUT3 (c) and FasL (f) genes, GLUT4-specific primers were used to amplify several exon-exon (e.g. Ex7-Ex8), exon-intron (e.g. Ex4-In4/5) and intra-intronic (e.g. In2/3) segments of the two major RNA splicing variants examined ( (d-f) (also, see Additional file 5: Figure S5 and Additional file 9: Table S1). GAPDH served as gene of reference. Ex: (single) exon. In: intron (in-between successive exons). Sv001/Sv004: GLUT4 RNA splicing variants

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