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Figure 5 | Breast Cancer Research

Figure 5

From: Targeting cholesterol-rich microdomains to circumvent tamoxifen-resistant breast cancer

Figure 5

Combination of α-TEA + TAM acts cooperatively to reduce prosurvival signaling in TAMR cells. (a, b) Western immunoblot analyses using aliquots of cell lysates from treated cells in Figure 3b were performed to assess prosurvival signaling mediators (a) and to assess antiapoptotic factors c-FLIP and Bcl-2 protein expression (b). (c) MCF-7/TAMR cells transfected with siRNAs to Akt-1 or c-FLIP, as well as control siRNA (labeled Control), were treated with α-TEA (20 μM) for 1 day. Western immunoblot analyses were performed to determine PARP, pJNK2/1, CHOP, DR5 (L/S), GRP 78, pAKT, and c-FLIP protein levels, with GAPDH serving as loading control. (a-c) Data are representative of three individual experiments. α-TEA, RRR-α-tocopherol ether-linked acetic acid analogue; Bcl-2, B-cell lymphoma 2; c-FLIP, cellular FLICE-inhibitory protein; CHOP, Ccaat-enhancer-binding protein (C/EBP) homologous protein; DR5 (L/S), death receptor 5 long/short; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GRP78, glucose-regulated protein-78; MCF-7/TAMR, acquired tamoxifen-resistant MCF-7; pJNK, phosphorylated-c-Jun N-terminal kinase; siRNA, small interfering RNA; TAM, tamoxifen; TAMR, tamoxifen resistant.

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