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1.
Figure 5

Figure 5. From: ASC-J9 Suppresses Castration-Resistant Prostate Cancer Growth through Degradation of Full-length and Splice Variant Androgen Receptors.

Knocking-down AR3 suppresses AR-targeted genes and cell growth in CWR22Rv1 and CWR22Rv1-fARKD cells. (A) Reduction of AR3 expression after delivery of shAR3. We evaluated the shAR3 knockdown efficiency by Western blot analysis in CWR22Rv1 and CWR22Rv1-fARKD cells. (B) Examination of AR-targeted gene expressions after AR3 knockdown. CWR22Rv1 and CWR22Rv1-fARKD cells with scramble control or shAR3 expression were used to detect AR-targeted gene expression by real-time PCR. (C) Effect of AR3 on cell growth of CWR22Rv1 and CWR22Rv1-fARKD cells. CWR22Rv1 and CWR22Rv1-fARKD cells infected with control (solid line) or shAR3 (dashed line) were treated with 1 nM DHT and ASC-J9 followed by MTT cell growth assay. Data presented are from at least three independent experiments.

Shinichi Yamashita, et al. Neoplasia. 2012 January;14(1):74-83.
2.
Figure 1

Figure 1. From: ASC-J9 Suppresses Castration-Resistant Prostate Cancer Growth through Degradation of Full-length and Splice Variant Androgen Receptors.

Little suppressive effect of Casodex on CRPC cells with AR3 expression. (A) AR expression in CRPC cell lines. Cell lysates of C81, C4-2, and CWR22Rv1 (22Rv1) cells were immunoblotted with anti-AR and anti-GAPDH. (B) AR3 expression in C81/AR3 and C4-2/AR3 cells. C81 and C4-2 cells were infected with lentiviral vector pWPI/AR3 and the expression of AR3 was confirmed by Western blot analysis. (C) Effect of Casodex on cell growth. CWR22Rv1 (left panel), C4-2/Vector (middle panel), and C4-2/AR3 (right panel) cells were treated with 5 or 10 µM Casodex, and the cell growth was examined by MTT assay. Data presented are from at least three independent experiments.

Shinichi Yamashita, et al. Neoplasia. 2012 January;14(1):74-83.
3.
Figure 2

Figure 2. From: ASC-J9 Suppresses Castration-Resistant Prostate Cancer Growth through Degradation of Full-length and Splice Variant Androgen Receptors.

Increased AR3 expression in CRPC of human PCa specimens. (A) Human prostate tumor tissues of the same patient were immunostained with specific AR3 (AR-V7) antibody. Representative data shown are from six pairs of patients before and after ADT. Scale bar, 50 µm. (B) The immunoreactive score of AR3 expression was determined. Six paired human prostate tissues were evaluated and represented by negative, weak, moderate, and strong expression as 0, 1, 2, and 3, respectively. *P < .05 and **P < .01, Student's t test.

Shinichi Yamashita, et al. Neoplasia. 2012 January;14(1):74-83.
4.
Figure 4

Figure 4. From: ASC-J9 Suppresses Castration-Resistant Prostate Cancer Growth through Degradation of Full-length and Splice Variant Androgen Receptors.

ASC-J9 suppresses AR-targeted genes and cell growth by degradation of fAR and ectopic AR3 in C81 and C4-2 cells. (A) Determination of fAR and AR3 expression after ASC-J9 treatment. C81 and C4-2 cells infected with pWPI/AR3 or vector alone were treated with 10 µM ASC-J9 and vehicle or 1 nM DHT for 24 hours. AR expression was evaluated by Western blot analysis. (B) Expressions of AR-targeted genes in AR3 overexpressed cells. C81 and C4-2 cells with ectopically expressed AR3 were treated with ASC-J9. The expressions of AR-targeted genes, such as PSA, TMPRSS2, and FKBP5, were evaluated by real-time PCR. (C) Effects of ASC-J9 on cell growth of C81/Vector, C81/AR3, C4-2/ Vector, and C4-2/AR3 cells were examined by MTT assay. Data presented are from at least three independent experiments.

Shinichi Yamashita, et al. Neoplasia. 2012 January;14(1):74-83.
5.
Figure 6

Figure 6. From: ASC-J9 Suppresses Castration-Resistant Prostate Cancer Growth through Degradation of Full-length and Splice Variant Androgen Receptors.

Therapeutic effect of ASC-J9 in vivo. (A) Evaluation of tumor volumes of CWR22Rv1 xenografts after ASC-J9 treatment. CWR22Rv1 cells were implanted into anterior prostates of castrated nude mice (four mice each group) and ASC-J9 was intraperitoneally injected for 4 weeks. Orthotopic tumors were harvested (eight tumors each group). Tumor volumes were measured and presented as mean ± SEM. Comparison among groups was performed using Student's t test. (B) Body weight determination during ASC-J9 treatment. Body weights were weekly measured in vehicle- or ASC-J9-injected mice. (C) Histologic examination of tumor tissues after ASC-J9 treatment. The tissues of xenografted tumors were processed by hematoxylin-eosin (HE) staining and immunohistochemical staining for AR, Ki67, and TUNEL. Representative data shown are from four tumors in the ASC-J9 and control groups. Arrows indicate TUNEL-positive cells. Scale bar, 50 µm. (D) Decreased AR expression of CWR22Rv1-xenografted tumors after ASC-J9 treatment. Proteins were harvested from three tumors of each group. AR expression was evaluated by Western blot analysis. (E) Quantification of Ki67 and TUNEL-positive cells in xenografted tumors. The ratio of immunostained positive cells (%) was calculated by the formula: (the number of positive cells/total number of counted cells) x 100. Comparisons among groups were performed using Student's t test.

Shinichi Yamashita, et al. Neoplasia. 2012 January;14(1):74-83.
6.
Figure 3

Figure 3. From: ASC-J9 Suppresses Castration-Resistant Prostate Cancer Growth through Degradation of Full-length and Splice Variant Androgen Receptors.

ASC-J9 suppresses AR-targeted genes, AR transactivation, and cell growth through AR degradation in CRPC cells. (A) Degradation of fAR and AR3 by ASC-J9. CRPC cells were treated with 5, 7.5, and 10 µM ASC-J9 in the presence or absence of 1 nM DHT for 24 hours. The expression of fAR and AR3 was evaluated by Western blot analysis in C81 (upper panel), C4-2 (middle panel), CWR22Rv1 (lower panel), and CWR22Rv1-fARKD (bottom panel). (B) Reduction of AR-targeted gene expression after ASC-J9 treatment. C81, C4-2, CWR22Rv1, and CWR22Rv1-fARKD cells were treated with 10 µM ASC-J9. The expressions of AR-targeted genes PSA (upper panel), TMPRSS2 (middle panel), and FKBP5 (lower panel) were determined by real-time PCR analysis. (C) Suppressive effect of ASC-J9 on AR transactivation in CRPC cells. AR transactivational activity was monitored by transfection of MMTV-Luc (upper panel) or ARE4-Luc (lower panel) into C81, C4-2, and CWR22Rv1 cells and treating with 10 µM ASC-J9. The results were normalized to Renilla luciferase and presented as fold difference between groups. (D) Effect of ASC-J9 on cell growth was determined by MTT assay. (E) Elevated cell cycle regulators p21 and p27 in ASC-J9-treated CWR22Rv1 cells leading to inhibition of cell growth. The expressions of fAR/AR3, proliferating cell nuclear antigen (PCNA), p21, p27, and GAPDH were evaluated by Western blot analysis. Data presented are from at least three independent experiments.

Shinichi Yamashita, et al. Neoplasia. 2012 January;14(1):74-83.

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