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sch772984  (MedChemExpress)


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    MedChemExpress sch772984
    PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM <t>SCH772984,</t> 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .
    Sch772984, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 286 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Targeting the noncanonical function of metabolic enzyme PHGDH in driving PD-L1 expression and cancer immune evasion"

    Article Title: Targeting the noncanonical function of metabolic enzyme PHGDH in driving PD-L1 expression and cancer immune evasion

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2026.102704

    PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM SCH772984, 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .
    Figure Legend Snippet: PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM SCH772984, 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .

    Techniques Used: Expressing, Western Blot, Activation Assay, Knockdown



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    PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM <t>SCH772984,</t> 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .
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    PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM <t>SCH772984,</t> 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .
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    PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM <t>SCH772984,</t> 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .
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    PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM SCH772984, 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .

    Journal: Cell Reports Medicine

    Article Title: Targeting the noncanonical function of metabolic enzyme PHGDH in driving PD-L1 expression and cancer immune evasion

    doi: 10.1016/j.xcrm.2026.102704

    Figure Lengend Snippet: PHGDH upregulates PD-L1 expression through the RAF1-MEK/ERK pathway to promote tumorigenesis in mice (A) Western blot analysis of RAF1-MEK/ERK signaling following PHGDH KO in cells. p-RAF1: p-RAF1 (Ser338), p-MEK1/2: p-MEK1/2 (Ser217/221), and p-ERK1/2: p-ERK1/2 (Thr202/Tyr204). (B) Activation of RAF1-MEK/ERK signaling by ectopic PHGDH-Flag expression in cells. (C) Effect of RAF1 knockdown on PHGDH-mediated MEK/ERK activation and PD-L1 upregulation in cells. (D and E) MEK inhibitors (15 μM U0126, 1 μM PD98059) and ERK inhibitors (1 μM SCH772984, 25 nM LY3214996) largely abolished PHGDH-induced PD-L1 expression. Cells were treated for 16 h. (F) The weights of MC38 and CT26 syngeneic tumors formed by cells with KO of PHGDH, RAF1, PD-L1, or their combinations. (G) Western blot analysis of tumors described in F. At least 6 tumors/group were analyzed, and similar results were observed. (H) Western blot analysis of MC38 and CT26 cells with the indicated genetic deletions, with or without PHGDH-Flag expression. (I) The weights of MC38 and CT26 syngeneic tumors established by cells as described in (H) in mice treated with or without the PHGDH inhibitor NCT-503 (50 mg/kg/day; intraperitoneally [i.p.]; for 12 days starting the day after cell inoculation). (J) Schematic model showing that PHGDH promotes PD-L1 expression and tumorigenesis by activating the RAF1-MEK/ERK pathway. In (F–I), tumors were collected at day 18 after cell inoculation. n = 10 mice/group, two-way ANOVA followed by Tukey’s test. # p < 0.05; ∗∗∗ p < 0.0001. See also , , , , and .

    Article Snippet: SCH772984 , MedChemExpress , Cat# HY-50846.

    Techniques: Expressing, Western Blot, Activation Assay, Knockdown