Bortezomib increases miR-29b and decreases oncogene expression in vivo. (A) Clinical images of representative IL-15 transgenic CTCL mice treated intraperitoneally with PBS vehicle (above) or 1 mg/kg bortezomib (below) for 5 weeks. (B) Photomicrographs of skin from representative IL-15 transgenic CTCL mice treated with vehicle (PBS/dimethyl sulfoxide) or bortezomib. Hematoxylin and eosin stain (40×, left; 400×, right). (C) Histology lesion severity score of skin tissue from mice treated with vehicle (n = 4) or bortezomib (n = 4). (D) Counts of CD3⁺ cells within surface and follicular epithelium (left) and within the superficial dermis (right) in vehicle-treated and bortezomib-treated mice. (E) Counts of CD4⁺ cells within surface and follicular epithelium (left) and within the superficial dermis (right) in vehicle-treated and bortezomib-treated mice. (F) RT-PCR of pri-miR-29b1 in blood of bortezomib-treated mice (n = 4) compared with vehicle-treated mice (n = 4). (G) Immunoblot analysis of BRD4, NOTCH1, and RBPJ from skin tissue of IL-15 transgenic CTCL mice treated with vehicle or 1 mg/kg bortezomib, with actin as an internal control. (H) Immunoblot of NOTCH1 and RBPJ protein expression in splenocytes from miR-29b^−/− mice compared with that of age-matched WT mice. Data are presented as mean ± SEM unless otherwise specified. *P ≤ .05; **P ≤ .01; ***P ≤ .001; ****P ≤ .0001; unpaired 2-tailed Student t test.