paradol  (MedChemExpress)


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    MedChemExpress paradol
    <t>6-Paradol-mediated</t> ubiquitination degradation of EGFR leads to inactivate PI3K/AKT signaling pathway. A The effect of 6-Paradol on EGFR mRNA by PCR analysis. B , C The effect of 6-Paradol on protein stability of EGFR was measured using 293 T cells treated with CHX for 1 h or 2 h. D A proteasome inhibitor, MG-132 (5 μM), was used to evaluate whether 6-Paradol was involved in EGFR degradation by a proteasome-dependent route. E Co-immunoprecipitation and SDS-gel electrophoresis were performed to evaluate the levels of EGFR ubiquitination in 293 T cells. F , G Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol and EGFR overexpressed plasmid. H Immunofluorescence analysis of p-AKT levels in the 6-P and NC groups in MIA PaCa-2 and SW1990 cells. ** p
    Paradol, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/paradol/product/MedChemExpress
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    paradol - by Bioz Stars, 2022-07
    86/100 stars

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    1) Product Images from "[6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling"

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    Journal: Cancer Cell International

    doi: 10.1186/s12935-021-02118-0

    6-Paradol-mediated ubiquitination degradation of EGFR leads to inactivate PI3K/AKT signaling pathway. A The effect of 6-Paradol on EGFR mRNA by PCR analysis. B , C The effect of 6-Paradol on protein stability of EGFR was measured using 293 T cells treated with CHX for 1 h or 2 h. D A proteasome inhibitor, MG-132 (5 μM), was used to evaluate whether 6-Paradol was involved in EGFR degradation by a proteasome-dependent route. E Co-immunoprecipitation and SDS-gel electrophoresis were performed to evaluate the levels of EGFR ubiquitination in 293 T cells. F , G Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol and EGFR overexpressed plasmid. H Immunofluorescence analysis of p-AKT levels in the 6-P and NC groups in MIA PaCa-2 and SW1990 cells. ** p
    Figure Legend Snippet: 6-Paradol-mediated ubiquitination degradation of EGFR leads to inactivate PI3K/AKT signaling pathway. A The effect of 6-Paradol on EGFR mRNA by PCR analysis. B , C The effect of 6-Paradol on protein stability of EGFR was measured using 293 T cells treated with CHX for 1 h or 2 h. D A proteasome inhibitor, MG-132 (5 μM), was used to evaluate whether 6-Paradol was involved in EGFR degradation by a proteasome-dependent route. E Co-immunoprecipitation and SDS-gel electrophoresis were performed to evaluate the levels of EGFR ubiquitination in 293 T cells. F , G Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol and EGFR overexpressed plasmid. H Immunofluorescence analysis of p-AKT levels in the 6-P and NC groups in MIA PaCa-2 and SW1990 cells. ** p

    Techniques Used: Polymerase Chain Reaction, Immunoprecipitation, SDS-Gel, Electrophoresis, Western Blot, Expressing, Plasmid Preparation, Immunofluorescence

    Schematic diagram of mechanism. [6]-Paradol inhibited pancreatic cancer cell proliferation and migration and inhibited the activation of PI3K/AKT signaling by targeting EGFR and enhancing EGFR degradation via a proteasome-dependent route
    Figure Legend Snippet: Schematic diagram of mechanism. [6]-Paradol inhibited pancreatic cancer cell proliferation and migration and inhibited the activation of PI3K/AKT signaling by targeting EGFR and enhancing EGFR degradation via a proteasome-dependent route

    Techniques Used: Migration, Activation Assay

    EGFR inhibitor enhanced 6-Paradol mediated-inhibition effect on PI3K/AKT signaling activity. A , B Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol, EGFR overexpressed plasmid and Erlotinib (2 nM). C – F Gain- or Lose-Functional experiments were performed to measure the proliferation and migration abilities of pancreatic cancer cells, which were respectively treated with 6-Paradol, EGFR overexpressed plasmid and (or) Erlotinib (2 nM). G , H The protein expression changes of E-cadherin, N-cadherin and Vimentin in Control, 6-P, 6-P + Erlotinib and 6-P + Erlotinib + EGFR groups, respectively. * p
    Figure Legend Snippet: EGFR inhibitor enhanced 6-Paradol mediated-inhibition effect on PI3K/AKT signaling activity. A , B Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol, EGFR overexpressed plasmid and Erlotinib (2 nM). C – F Gain- or Lose-Functional experiments were performed to measure the proliferation and migration abilities of pancreatic cancer cells, which were respectively treated with 6-Paradol, EGFR overexpressed plasmid and (or) Erlotinib (2 nM). G , H The protein expression changes of E-cadherin, N-cadherin and Vimentin in Control, 6-P, 6-P + Erlotinib and 6-P + Erlotinib + EGFR groups, respectively. * p

    Techniques Used: Inhibition, Activity Assay, Western Blot, Expressing, Plasmid Preparation, Functional Assay, Migration

    6-Paradol significantly suppressed tumor growth in vivo. A Tumor photographs of the subcutaneous xenografts in Control and 6-Paradol treatment groups, n = 5, cell line: SW1990. B Tumor volume of the subcutaneous xenografts in Control and 6-Paradol treatment groups. C Weight change curve in Control and 6-Paradol treatment groups. D IHC staining for Ki67, PCNA, EMT markers, EGFR, p-AKT and p-PI3K, and representative images of two pairs of subcutaneous xenograft tissue (100 ×). (Scale bar: 100 μm) * p
    Figure Legend Snippet: 6-Paradol significantly suppressed tumor growth in vivo. A Tumor photographs of the subcutaneous xenografts in Control and 6-Paradol treatment groups, n = 5, cell line: SW1990. B Tumor volume of the subcutaneous xenografts in Control and 6-Paradol treatment groups. C Weight change curve in Control and 6-Paradol treatment groups. D IHC staining for Ki67, PCNA, EMT markers, EGFR, p-AKT and p-PI3K, and representative images of two pairs of subcutaneous xenograft tissue (100 ×). (Scale bar: 100 μm) * p

    Techniques Used: In Vivo, Immunohistochemistry, Staining

    The chemical structural formulas of extracts of ginger. A [6]-Paradol. B [6]-Shogaol. C [6]-Gingerol
    Figure Legend Snippet: The chemical structural formulas of extracts of ginger. A [6]-Paradol. B [6]-Shogaol. C [6]-Gingerol

    Techniques Used:

    Inhibition of 6-Paradol on proliferation of pancreatic cancer cells. A , B CCK-8 assays were performed to measure proliferation ability of MIA PaCa-2 ( A ) and SW1990 ( B ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). C , D Colony formation assay was performed to test the cell colony ability in MIA PaCa-2 ( C ) and SW1990 ( D ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). E , F The pancreatic cancer cells were treated with different concentrations of 6-P for 48 h (0, 20, 40, 80 μM) or the same concentration of 6-P for different time frames (0, 24, 48, 72 h). And the morphological changes of MIA PaCa-2 E and SW1990 F were captured using a phase contrast microscope (scale bar: 200 μm). * p
    Figure Legend Snippet: Inhibition of 6-Paradol on proliferation of pancreatic cancer cells. A , B CCK-8 assays were performed to measure proliferation ability of MIA PaCa-2 ( A ) and SW1990 ( B ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). C , D Colony formation assay was performed to test the cell colony ability in MIA PaCa-2 ( C ) and SW1990 ( D ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). E , F The pancreatic cancer cells were treated with different concentrations of 6-P for 48 h (0, 20, 40, 80 μM) or the same concentration of 6-P for different time frames (0, 24, 48, 72 h). And the morphological changes of MIA PaCa-2 E and SW1990 F were captured using a phase contrast microscope (scale bar: 200 μm). * p

    Techniques Used: Inhibition, CCK-8 Assay, Colony Assay, Concentration Assay, Microscopy

    6-Paradol interacts with EGFR to exert suppression functions on proliferation and metastasis of pancreatic cancer cells. A PI3K-AKT signaling pathway and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance were correlated with 6-Paradol using KEGG pathway enrichment analysis. B The 3D structure of molecular docking between 6-Paradol and EGFR. C , D Western blot assays were performed to measure the effect of 6-Paradol (80 μM) on EGFR protein levels. E – G Gain-Functional experiment was performed to measure the effect of 6-Paradol (80 μM) on proliferation and migration of 6-P + EGFR group in MIA PaCa-2 and SW1990 (scale bar: 100 μm). H , I Western blot was applied to investigate effect of 6-P combined with EGFR on EMT transition in MIA PaCa-2 and PANC-1. ** p
    Figure Legend Snippet: 6-Paradol interacts with EGFR to exert suppression functions on proliferation and metastasis of pancreatic cancer cells. A PI3K-AKT signaling pathway and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance were correlated with 6-Paradol using KEGG pathway enrichment analysis. B The 3D structure of molecular docking between 6-Paradol and EGFR. C , D Western blot assays were performed to measure the effect of 6-Paradol (80 μM) on EGFR protein levels. E – G Gain-Functional experiment was performed to measure the effect of 6-Paradol (80 μM) on proliferation and migration of 6-P + EGFR group in MIA PaCa-2 and SW1990 (scale bar: 100 μm). H , I Western blot was applied to investigate effect of 6-P combined with EGFR on EMT transition in MIA PaCa-2 and PANC-1. ** p

    Techniques Used: Western Blot, Functional Assay, Migration

    Inhibition of 6-Paradol on migration and invasion of pancreatic cancer cells. A – D Transwell assays were performed to evaluate the migration and invasion abilities of pancreatic cancer cells and the cells were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). Migration abilities were evaluated without Matrigel ( A ) and invasion abilities were evaluated with Matrigel ( B ) (scale bar: 100 μm). The statistical chart of migration cells ( C ) and invasion cells ( D ) in different concentrations of 6-Paradol. E – G Wound healing assays were performed to further measure the migrated abilities in MIA PaCa-2 and SW1990 (scale bar: 400 μm). H , I Western blot assays were used to analyze the effect of 6-Paradol on EMT. * p
    Figure Legend Snippet: Inhibition of 6-Paradol on migration and invasion of pancreatic cancer cells. A – D Transwell assays were performed to evaluate the migration and invasion abilities of pancreatic cancer cells and the cells were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). Migration abilities were evaluated without Matrigel ( A ) and invasion abilities were evaluated with Matrigel ( B ) (scale bar: 100 μm). The statistical chart of migration cells ( C ) and invasion cells ( D ) in different concentrations of 6-Paradol. E – G Wound healing assays were performed to further measure the migrated abilities in MIA PaCa-2 and SW1990 (scale bar: 400 μm). H , I Western blot assays were used to analyze the effect of 6-Paradol on EMT. * p

    Techniques Used: Inhibition, Migration, Western Blot

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    MedChemExpress paradol
    <t>6-Paradol-mediated</t> ubiquitination degradation of EGFR leads to inactivate PI3K/AKT signaling pathway. A The effect of 6-Paradol on EGFR mRNA by PCR analysis. B , C The effect of 6-Paradol on protein stability of EGFR was measured using 293 T cells treated with CHX for 1 h or 2 h. D A proteasome inhibitor, MG-132 (5 μM), was used to evaluate whether 6-Paradol was involved in EGFR degradation by a proteasome-dependent route. E Co-immunoprecipitation and SDS-gel electrophoresis were performed to evaluate the levels of EGFR ubiquitination in 293 T cells. F , G Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol and EGFR overexpressed plasmid. H Immunofluorescence analysis of p-AKT levels in the 6-P and NC groups in MIA PaCa-2 and SW1990 cells. ** p
    Paradol, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/paradol/product/MedChemExpress
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    paradol - by Bioz Stars, 2022-07
    86/100 stars
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    6-Paradol-mediated ubiquitination degradation of EGFR leads to inactivate PI3K/AKT signaling pathway. A The effect of 6-Paradol on EGFR mRNA by PCR analysis. B , C The effect of 6-Paradol on protein stability of EGFR was measured using 293 T cells treated with CHX for 1 h or 2 h. D A proteasome inhibitor, MG-132 (5 μM), was used to evaluate whether 6-Paradol was involved in EGFR degradation by a proteasome-dependent route. E Co-immunoprecipitation and SDS-gel electrophoresis were performed to evaluate the levels of EGFR ubiquitination in 293 T cells. F , G Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol and EGFR overexpressed plasmid. H Immunofluorescence analysis of p-AKT levels in the 6-P and NC groups in MIA PaCa-2 and SW1990 cells. ** p

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: 6-Paradol-mediated ubiquitination degradation of EGFR leads to inactivate PI3K/AKT signaling pathway. A The effect of 6-Paradol on EGFR mRNA by PCR analysis. B , C The effect of 6-Paradol on protein stability of EGFR was measured using 293 T cells treated with CHX for 1 h or 2 h. D A proteasome inhibitor, MG-132 (5 μM), was used to evaluate whether 6-Paradol was involved in EGFR degradation by a proteasome-dependent route. E Co-immunoprecipitation and SDS-gel electrophoresis were performed to evaluate the levels of EGFR ubiquitination in 293 T cells. F , G Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol and EGFR overexpressed plasmid. H Immunofluorescence analysis of p-AKT levels in the 6-P and NC groups in MIA PaCa-2 and SW1990 cells. ** p

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques: Polymerase Chain Reaction, Immunoprecipitation, SDS-Gel, Electrophoresis, Western Blot, Expressing, Plasmid Preparation, Immunofluorescence

    Schematic diagram of mechanism. [6]-Paradol inhibited pancreatic cancer cell proliferation and migration and inhibited the activation of PI3K/AKT signaling by targeting EGFR and enhancing EGFR degradation via a proteasome-dependent route

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: Schematic diagram of mechanism. [6]-Paradol inhibited pancreatic cancer cell proliferation and migration and inhibited the activation of PI3K/AKT signaling by targeting EGFR and enhancing EGFR degradation via a proteasome-dependent route

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques: Migration, Activation Assay

    EGFR inhibitor enhanced 6-Paradol mediated-inhibition effect on PI3K/AKT signaling activity. A , B Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol, EGFR overexpressed plasmid and Erlotinib (2 nM). C – F Gain- or Lose-Functional experiments were performed to measure the proliferation and migration abilities of pancreatic cancer cells, which were respectively treated with 6-Paradol, EGFR overexpressed plasmid and (or) Erlotinib (2 nM). G , H The protein expression changes of E-cadherin, N-cadherin and Vimentin in Control, 6-P, 6-P + Erlotinib and 6-P + Erlotinib + EGFR groups, respectively. * p

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: EGFR inhibitor enhanced 6-Paradol mediated-inhibition effect on PI3K/AKT signaling activity. A , B Western blot assay was performed to measure the protein expression levels of PI3K/AKT signaling in MIA PaCa-2 and SW1990 cells treated with 6-Paradol, EGFR overexpressed plasmid and Erlotinib (2 nM). C – F Gain- or Lose-Functional experiments were performed to measure the proliferation and migration abilities of pancreatic cancer cells, which were respectively treated with 6-Paradol, EGFR overexpressed plasmid and (or) Erlotinib (2 nM). G , H The protein expression changes of E-cadherin, N-cadherin and Vimentin in Control, 6-P, 6-P + Erlotinib and 6-P + Erlotinib + EGFR groups, respectively. * p

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques: Inhibition, Activity Assay, Western Blot, Expressing, Plasmid Preparation, Functional Assay, Migration

    6-Paradol significantly suppressed tumor growth in vivo. A Tumor photographs of the subcutaneous xenografts in Control and 6-Paradol treatment groups, n = 5, cell line: SW1990. B Tumor volume of the subcutaneous xenografts in Control and 6-Paradol treatment groups. C Weight change curve in Control and 6-Paradol treatment groups. D IHC staining for Ki67, PCNA, EMT markers, EGFR, p-AKT and p-PI3K, and representative images of two pairs of subcutaneous xenograft tissue (100 ×). (Scale bar: 100 μm) * p

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: 6-Paradol significantly suppressed tumor growth in vivo. A Tumor photographs of the subcutaneous xenografts in Control and 6-Paradol treatment groups, n = 5, cell line: SW1990. B Tumor volume of the subcutaneous xenografts in Control and 6-Paradol treatment groups. C Weight change curve in Control and 6-Paradol treatment groups. D IHC staining for Ki67, PCNA, EMT markers, EGFR, p-AKT and p-PI3K, and representative images of two pairs of subcutaneous xenograft tissue (100 ×). (Scale bar: 100 μm) * p

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques: In Vivo, Immunohistochemistry, Staining

    The chemical structural formulas of extracts of ginger. A [6]-Paradol. B [6]-Shogaol. C [6]-Gingerol

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: The chemical structural formulas of extracts of ginger. A [6]-Paradol. B [6]-Shogaol. C [6]-Gingerol

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques:

    Inhibition of 6-Paradol on proliferation of pancreatic cancer cells. A , B CCK-8 assays were performed to measure proliferation ability of MIA PaCa-2 ( A ) and SW1990 ( B ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). C , D Colony formation assay was performed to test the cell colony ability in MIA PaCa-2 ( C ) and SW1990 ( D ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). E , F The pancreatic cancer cells were treated with different concentrations of 6-P for 48 h (0, 20, 40, 80 μM) or the same concentration of 6-P for different time frames (0, 24, 48, 72 h). And the morphological changes of MIA PaCa-2 E and SW1990 F were captured using a phase contrast microscope (scale bar: 200 μm). * p

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: Inhibition of 6-Paradol on proliferation of pancreatic cancer cells. A , B CCK-8 assays were performed to measure proliferation ability of MIA PaCa-2 ( A ) and SW1990 ( B ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). C , D Colony formation assay was performed to test the cell colony ability in MIA PaCa-2 ( C ) and SW1990 ( D ), which were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). E , F The pancreatic cancer cells were treated with different concentrations of 6-P for 48 h (0, 20, 40, 80 μM) or the same concentration of 6-P for different time frames (0, 24, 48, 72 h). And the morphological changes of MIA PaCa-2 E and SW1990 F were captured using a phase contrast microscope (scale bar: 200 μm). * p

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques: Inhibition, CCK-8 Assay, Colony Assay, Concentration Assay, Microscopy

    6-Paradol interacts with EGFR to exert suppression functions on proliferation and metastasis of pancreatic cancer cells. A PI3K-AKT signaling pathway and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance were correlated with 6-Paradol using KEGG pathway enrichment analysis. B The 3D structure of molecular docking between 6-Paradol and EGFR. C , D Western blot assays were performed to measure the effect of 6-Paradol (80 μM) on EGFR protein levels. E – G Gain-Functional experiment was performed to measure the effect of 6-Paradol (80 μM) on proliferation and migration of 6-P + EGFR group in MIA PaCa-2 and SW1990 (scale bar: 100 μm). H , I Western blot was applied to investigate effect of 6-P combined with EGFR on EMT transition in MIA PaCa-2 and PANC-1. ** p

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: 6-Paradol interacts with EGFR to exert suppression functions on proliferation and metastasis of pancreatic cancer cells. A PI3K-AKT signaling pathway and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance were correlated with 6-Paradol using KEGG pathway enrichment analysis. B The 3D structure of molecular docking between 6-Paradol and EGFR. C , D Western blot assays were performed to measure the effect of 6-Paradol (80 μM) on EGFR protein levels. E – G Gain-Functional experiment was performed to measure the effect of 6-Paradol (80 μM) on proliferation and migration of 6-P + EGFR group in MIA PaCa-2 and SW1990 (scale bar: 100 μm). H , I Western blot was applied to investigate effect of 6-P combined with EGFR on EMT transition in MIA PaCa-2 and PANC-1. ** p

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques: Western Blot, Functional Assay, Migration

    Inhibition of 6-Paradol on migration and invasion of pancreatic cancer cells. A – D Transwell assays were performed to evaluate the migration and invasion abilities of pancreatic cancer cells and the cells were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). Migration abilities were evaluated without Matrigel ( A ) and invasion abilities were evaluated with Matrigel ( B ) (scale bar: 100 μm). The statistical chart of migration cells ( C ) and invasion cells ( D ) in different concentrations of 6-Paradol. E – G Wound healing assays were performed to further measure the migrated abilities in MIA PaCa-2 and SW1990 (scale bar: 400 μm). H , I Western blot assays were used to analyze the effect of 6-Paradol on EMT. * p

    Journal: Cancer Cell International

    Article Title: [6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

    doi: 10.1186/s12935-021-02118-0

    Figure Lengend Snippet: Inhibition of 6-Paradol on migration and invasion of pancreatic cancer cells. A – D Transwell assays were performed to evaluate the migration and invasion abilities of pancreatic cancer cells and the cells were treated with different concentrations of 6-Paradol (0, 20, 40, 80 μM). Migration abilities were evaluated without Matrigel ( A ) and invasion abilities were evaluated with Matrigel ( B ) (scale bar: 100 μm). The statistical chart of migration cells ( C ) and invasion cells ( D ) in different concentrations of 6-Paradol. E – G Wound healing assays were performed to further measure the migrated abilities in MIA PaCa-2 and SW1990 (scale bar: 400 μm). H , I Western blot assays were used to analyze the effect of 6-Paradol on EMT. * p

    Article Snippet: P (No. HY-14617), MG-132 (No.HY-13259) and erlotinib (No. HY-50896) were purchased from the MedChemExpress (MCE, USA).

    Techniques: Inhibition, Migration, Western Blot