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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 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