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egfr activator egf  (MedChemExpress)


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    MedChemExpress egfr activator egf
    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
    Egfr Activator Egf, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/egfr+activator+egf/EGF%2C+Mouse/pm39971923-51-7-27
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    Images

    1) Product Images from "Metformin inhibits the growth of SCLC cells by inducing autophagy and apoptosis via the suppression of EGFR and AKT signalling."

    Article Title: Metformin inhibits the growth of SCLC cells by inducing autophagy and apoptosis via the suppression of EGFR and AKT signalling.

    Journal: Scientific reports

    doi: 10.1038/s41598-025-87537-z

    Fig. 5. Metformin inhibits the EGFR/AKT/AMPK/mTOR axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), EGF (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
    Figure Legend Snippet: Fig. 5. Metformin inhibits the EGFR/AKT/AMPK/mTOR axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), EGF (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.

    Techniques Used: Western Blot, Binding Assay, Control

    Related Articles

    Western Blot:

    Article Title: Metformin inhibits the growth of SCLC cells by inducing autophagy and apoptosis via the suppression of EGFR and AKT signalling
    Article Snippet: The autophagy inhibitor 3-methyladenine (3-MA, HY-19312), the EGFR activator EGF (HY-P70590), the AMPK inhibitor compound C (HY-13418 A), and the AKT activator SC79 (HY-18749) were purchased from MedChemExpress (Shanghai, China).

    Binding Assay:

    Article Title: Metformin inhibits the growth of SCLC cells by inducing autophagy and apoptosis via the suppression of EGFR and AKT signalling
    Article Snippet: The autophagy inhibitor 3-methyladenine (3-MA, HY-19312), the EGFR activator EGF (HY-P70590), the AMPK inhibitor compound C (HY-13418 A), and the AKT activator SC79 (HY-18749) were purchased from MedChemExpress (Shanghai, China).

    Control:

    Article Title: Metformin inhibits the growth of SCLC cells by inducing autophagy and apoptosis via the suppression of EGFR and AKT signalling
    Article Snippet: The autophagy inhibitor 3-methyladenine (3-MA, HY-19312), the EGFR activator EGF (HY-P70590), the AMPK inhibitor compound C (HY-13418 A), and the AKT activator SC79 (HY-18749) were purchased from MedChemExpress (Shanghai, China).



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    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
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    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
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    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
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    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
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    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
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    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
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    Fig. 5. Metformin inhibits the <t>EGFR/AKT/AMPK/mTOR</t> axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), <t>EGF</t> (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.
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    Image Search Results


    Fig. 5. Metformin inhibits the EGFR/AKT/AMPK/mTOR axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), EGF (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.

    Journal: Scientific reports

    Article Title: Metformin inhibits the growth of SCLC cells by inducing autophagy and apoptosis via the suppression of EGFR and AKT signalling.

    doi: 10.1038/s41598-025-87537-z

    Figure Lengend Snippet: Fig. 5. Metformin inhibits the EGFR/AKT/AMPK/mTOR axis in SCLC cells. (A) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, p-AKT, EGFR, and p-EGFR were measured in H446, H446/DDP, H526, and H526/DDP cells treated with different concentrations of metformin for 48 h via western blotting. (B) The binding mode of metformin docked to EGFR. (C) ATP content of SCLC cells after treatment with metformin (0, 5, or 10 mM) for 48 h. Significant difference compared with the untreated control: *p < 0.05; **p < 0.01; ***p < 0.001. n = 3. (D) The protein levels of EGFR, p-EGFR, AKT, p-AKT, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), EGF (50 µg/ml), or metformin + EGF for 48 h. (E) The protein levels of AKT, p-AKT, mTOR, p-mTOR, AMPK, and p-AMPK were measured via western blotting in H446 and H446/DDP cells treated with metformin (10 mM), SC79 (4 µg/ml), or metformin + SC79 for 48 h. (F) The protein levels of AMPK, p-AMPK, mTOR, p-mTOR, AKT, and p-AKT were measured in H446 and H446/DDP cells treated with metformin (10 mM), compound C (2 µM), or metformin + Compound C for 48 h via western blotting.

    Article Snippet: The autophagy inhibitor 3-methyladenine (3-MA, HY-19312), the EGFR activator EGF (HY-P70590), the AMPK inhibitor compound C (HY-13418 A), and the AKT activator SC79 (HY-18749) were purchased from MedChemExpress (Shanghai, China).

    Techniques: Western Blot, Binding Assay, Control