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FIGURE 4 | Pamiparib treatment induces PD-L1 expression via <t>JAK2/STAT3</t> pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.
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FIGURE 4 | Pamiparib treatment induces PD-L1 expression via <t>JAK2/STAT3</t> pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.
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FIGURE 4 | Pamiparib treatment induces PD-L1 expression via <t>JAK2/STAT3</t> pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.
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FIGURE 4 | Pamiparib treatment induces PD-L1 expression via <t>JAK2/STAT3</t> pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.
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FIGURE 4 | Pamiparib treatment induces PD-L1 expression via <t>JAK2/STAT3</t> pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.
Anti Pjak2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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FIGURE 4 | Pamiparib treatment induces PD-L1 expression via <t>JAK2/STAT3</t> pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.
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The impacts of polydatin treatments on <t>JAK2</t> and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.
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The impacts of polydatin treatments on <t>JAK2</t> and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.
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Image Search Results


FIGURE 4 | Pamiparib treatment induces PD-L1 expression via JAK2/STAT3 pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.

Journal: Frontiers in immunology

Article Title: PARP Inhibitor Upregulates PD-L1 Expression and Provides a New Combination Therapy in Pancreatic Cancer.

doi: 10.3389/fimmu.2021.762989

Figure Lengend Snippet: FIGURE 4 | Pamiparib treatment induces PD-L1 expression via JAK2/STAT3 pathway. (A) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by immunoblotting after treatment with the concentrations (20 mM) of AG490 for 24h. (B) Cells were pretreated with pamiparib (100 mM, 12h) and PD-L1 expression was assessed by protein blotting after treatment with stattic (20 mM) for 24h. (C) Protein expression of phospho-JAK2 (p-JAK2), JAK2, and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. (D) Protein expression of phospho-STAT3(p-STAT3), STAT3 and PD-L1 in SW1990 cells after being treated with pamiparib (100 mM) for the indicated times. GAPDH was used as a loading control. (E) IHC staining of p-STAT3 of nude mouse xenograft tumors in control group and treated with pamiparib group. Scale bar, 100 mm. (F) IHC staining score showed the expression of p-STAT3 was significantly upregulated in nude mice pamiparib treated group. Data are mean ± SD; n = 3 samples per group. The IHC results were analyzed by Pearson c2 test. *P < 0.05.

Article Snippet: The primary antibodies are PD-L1 (CST #13684, Cell Signaling Technology), PD-L1 (17952- 1-AP, Santa Cruz), STAT3 (CST #9139, Cell Signaling Technology), phosphorylated STAT3 (CST #9145, Cell Signaling Technology), JAK2 (17670-1-AP, Proteintech), phosphorylated JAK2 (CST #4406, Cell Signaling Technology), AKT (10176-2-AP, Proteintech), phosphorylated AKT (66444-1-Ig, Proteintech), ERK (CST #4696, Cell Signaling Technology), phosphorylated ERK (CST #3510, Cell Signaling Technology), PARP-1 (sc-8007, Santa Cruz), and GAPDH (60004-1-Ig, Proteintech).

Techniques: Expressing, Western Blot, Control, Immunohistochemistry

FIGURE 8 | Diagram summarizing that pamiparib treatment induces PD-L1 expression mainly via JAK2/STAT3 in pancreatic cancer (details provided in the Discussion section).

Journal: Frontiers in immunology

Article Title: PARP Inhibitor Upregulates PD-L1 Expression and Provides a New Combination Therapy in Pancreatic Cancer.

doi: 10.3389/fimmu.2021.762989

Figure Lengend Snippet: FIGURE 8 | Diagram summarizing that pamiparib treatment induces PD-L1 expression mainly via JAK2/STAT3 in pancreatic cancer (details provided in the Discussion section).

Article Snippet: The primary antibodies are PD-L1 (CST #13684, Cell Signaling Technology), PD-L1 (17952- 1-AP, Santa Cruz), STAT3 (CST #9139, Cell Signaling Technology), phosphorylated STAT3 (CST #9145, Cell Signaling Technology), JAK2 (17670-1-AP, Proteintech), phosphorylated JAK2 (CST #4406, Cell Signaling Technology), AKT (10176-2-AP, Proteintech), phosphorylated AKT (66444-1-Ig, Proteintech), ERK (CST #4696, Cell Signaling Technology), phosphorylated ERK (CST #3510, Cell Signaling Technology), PARP-1 (sc-8007, Santa Cruz), and GAPDH (60004-1-Ig, Proteintech).

Techniques: Expressing

The impacts of polydatin treatments on JAK2 and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.

Journal: Annals of Translational Medicine

Article Title: Polydatin down-regulates the phosphorylation level of STAT3 and induces pyroptosis in triple-negative breast cancer mice with a high-fat diet

doi: 10.21037/atm-22-73

Figure Lengend Snippet: The impacts of polydatin treatments on JAK2 and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.

Article Snippet: The following primary antibodies were used: Rabbit anti-STAT3 antibody (1:1,000, Abcam, Cambridge, USA), Rabbit anti-JAK2 antibody [1:1,000, Cell Signaling Technology (CST), Danvers, MA, USA], rabbit anti-Phospho-STAT3 antibody (1:500, CST, USA), rabbit anti-IL1β antibody (1:500, Abcam, USA), rabbit anti-Phospho-JAK2 antibody (1:500, CST, USA), rabbit anti-pro Caspase-1 + p10 + p12 antibody (1:500, Abcam, USA), rabbit anti-Cleaved Caspase-3 antibody (1:1,000, CST, USA), rabbit anti-NLRP3 antibody (1:800, Abcam, USA), rabbit anti-IL18 antibody (1:500, Abcam, USA), rabbit anti-Caspase-3 antibody (1:1,000, CST, USA), rabbit anti-Caspase-1 antibody (1:500, Abcam, USA), rabbit anti-GSDMD antibody (1:500, Abcam, USA), rabbit anti-GAPDH antibody (1:3,000, Abcam, USA), and mouse β-actin monoclonal antibody (1:3,000, Abcam, USA).

Techniques: Expressing