ACP5 Antibody - #DF6989

Fig. 3 RANK regulated CRC migration and invasion by activating ACP5 expression. a, b Western blot analysis of upregulation of ACP5 protein in RANK-overexpressing SW480 and Caco2 cells, and downregulation of ACP5 protein in RANK knockdown HT29 cells. c, f Western blotting showed that successful decreased ACP5 protein in RANK overexpression CRC cells transfected with siRNA-ACP5 and increased ACP5 protein by transfection with pFV-ACP5 plasmid in RANK knockdown CRC cells. d, e Knockdown of ACP5 inhibited RANK-induced migration and invasion in SW480RK and Caco2RK cells. Scales bars = 100 μm. g, h ACP5 overexpression increased migration and invasion of RANK-silencing HT29 cells. Scales bars = 100 μm. i Representative immunofluorescence of ACP5 distribution in high and low RANK expression CRC tissues. Nuclei (blue) were counterstained with DAPI. The white arrowheads indicate ACP5-positive cells are distributed within the tumor and stroma with high RANK expression. + (score 1–4), +++ (score 9–12). Scales bars = 10 μm. Data are mean ± SD (n = 3).

Fig. 3 RANK regulated CRC migration and invasion by activating ACP5 expression. a, b Western blot analysis of upregulation of ACP5 protein in RANK-overexpressing SW480 and Caco2 cells, and downregulation of ACP5 protein in RANK knockdown HT29 cells. c, f Western blotting showed that successful decreased ACP5 protein in RANK overexpression CRC cells transfected with siRNA-ACP5 and increased ACP5 protein by transfection with pFV-ACP5 plasmid in RANK knockdown CRC cells. d, e Knockdown of ACP5 inhibited RANK-induced migration and invasion in SW480RK and Caco2RK cells. Scales bars = 100 μm. g, h ACP5 overexpression increased migration and invasion of RANK-silencing HT29 cells. Scales bars = 100 μm. i Representative immunofluorescence of ACP5 distribution in high and low RANK expression CRC tissues. Nuclei (blue) were counterstained with DAPI. The white arrowheads indicate ACP5-positive cells are distributed within the tumor and stroma with high RANK expression. + (score 1–4), +++ (score 9–12). Scales bars = 10 μm. Data are mean ± SD (n = 3).

Figure 1 AR can decrease the progression of HCC cells while ACP5 can increase. A-B. Western blot was used to check AR protein expression after shAR/oeAR in HCC cells. C-D. Wound-healing and transwell invasion assay was used to check the migration and invasion capacity in the HA22T shAR cells. E-F. Wound-healing and transwell invasion assay was used to check the migration and invasion capacity in the SK-HEP-1 oeAR cells. G-H. Western blot assay was used to check related protein expressions after over expression AR/knocking down AR in HCC cells. I-J. Western blot assay was used to check ACP5 expression after shACP5/oeACP5 in HCC cells. K-L. Wound-healing assay was used to check the migration capacity after shACP5/oeACP5 in HCC cells. M-N. Transwell invasion assay was used to check the invasion capacity after shACP5/oeACP5 in HCC cells. All quantifications are mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, ns: no significant difference.

Figure 4. |rSj‑Cys inhibits the expression of osteoclastogenesis‑related genes and proteins. RAW264.7 cells were co‑stimulated with M‑CSF (25 ng/ml) and RANKL (30 ng/ml) and then treated with or without rSj‑Cys (0.3 µM) for different time periods (24, 48 or 72 h). The expression levels of genes and proteins associated with osteoclast phenotype markers (CTSK, TRAP, ITGB3) and cell surface receptors of osteoclast precursors (RANK, OSCAR, TREM‑2)were determined by (A) reverse transcription‑quantitative PCR and (B) western blot analysis.

Figure 3 TsI restrains osteoclastogenesis in the femoral heads of the MPS-induced SIONFH rat model. (a) TRAP activity in the serum. (b) Expression levels of CTSK and ACP5 in the femoral heads. ∗∗p < 0.01; ns, no significant. TRAP, tartrate-resistant acid phosphatase; CTSK, cathepsin K; ACP5, acid phosphatase 5.