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MedChemExpress isoliquiritigenin isl
Original uncropped western blot bands used in this study. ( A ) Inhibition of PITX1 decreased the protein expression level of PFKP in the breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A), as revealed by western blot analysis. ( B ) Western blot analysis revealed downregulation of PFKP protein levels in breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A) after <t>isoliquiritigenin</t> treatment.
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MedChemExpress isl powder
Original uncropped western blot bands used in this study. ( A ) Inhibition of PITX1 decreased the protein expression level of PFKP in the breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A), as revealed by western blot analysis. ( B ) Western blot analysis revealed downregulation of PFKP protein levels in breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A) after <t>isoliquiritigenin</t> treatment.
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Tokyo Chemical Industry isoliquiritigenin
Chalcone derivatives inhibited TNF-α-induced ICAM-1 expression. ( A ) Structures of 4′-hydroxychalcone, <t>isoliquiritigenin,</t> and xanthohumol. ( B – G ) A549 cells were treated with 4′-hydroxychalcone ( B , E ), isoliquiritigenin ( C , F ), and xanthohumol ( D , G ) for 1 h, followed by a 6-h stimulation with (+) or without (−) TNF-α (2.5 ng/mL) in the presence or absence of 4′-hydroxychalcone, isoliquiritigenin, and xanthohumol (5–50 µM). Cell viability (%) (blue bars) is presented as the mean ± standard error ( n = 3) ( B – D ). No significant differences were observed ( B – D ). ICAM-1 expression (%) (magenta bars) is presented as the mean ± standard error ( n = 3) ( E – G ). *** p < 0.001.
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Original uncropped western blot bands used in this study. ( A ) Inhibition of PITX1 decreased the protein expression level of PFKP in the breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A), as revealed by western blot analysis. ( B ) Western blot analysis revealed downregulation of PFKP protein levels in breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A) after isoliquiritigenin treatment.

Journal: Oncology Research

Article Title: Isoliquiritigenin Impedes Breast Cancer Progression through PITX1–PFKP-Mediated Glycolysis Reprogramming

doi: 10.32604/or.2026.077059

Figure Lengend Snippet: Original uncropped western blot bands used in this study. ( A ) Inhibition of PITX1 decreased the protein expression level of PFKP in the breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A), as revealed by western blot analysis. ( B ) Western blot analysis revealed downregulation of PFKP protein levels in breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A) after isoliquiritigenin treatment.

Article Snippet: Isoliquiritigenin (ISL) was purchased from MedChemExpress (MCE, Monmouth Junction, NJ, USA; Cat. No. HY-N0373).

Techniques: Western Blot, Inhibition, Expressing

Isoliquiritigenin inhibits the proliferation and metastatic ability of breast cancer cells via targeting PITX1–PFKP-mediated glycolysis reprogramming. ( A ) Chemical structure of isoliquiritigenin. ( B ) Isoliquiritigenin treatment significantly downregulated PITX1 expression in breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A). ( C ) CCK-8 assay showing reduced proliferation rates in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells following isoliquiritigenin treatment. ( D , E ) Colony formation assays revealed that isoliquiritigenin significantly inhibited clonogenic potential in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells. ( F ) Transwell assays demonstrated reduced migratory capacity of MDA-MB-231 cells after isoliquiritigenin-induced PITX1 inhibition. Scale bar: 50 μm. ( G ) Glucose uptake was decreased in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells following isoliquiritigenin treatment. ( H ) Lactate production was reduced in all three cell lines upon PITX1 inhibition. ( I ) Western blot analysis revealed downregulation of PFKP protein levels in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells after isoliquiritigenin treatment. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Oncology Research

Article Title: Isoliquiritigenin Impedes Breast Cancer Progression through PITX1–PFKP-Mediated Glycolysis Reprogramming

doi: 10.32604/or.2026.077059

Figure Lengend Snippet: Isoliquiritigenin inhibits the proliferation and metastatic ability of breast cancer cells via targeting PITX1–PFKP-mediated glycolysis reprogramming. ( A ) Chemical structure of isoliquiritigenin. ( B ) Isoliquiritigenin treatment significantly downregulated PITX1 expression in breast cancer cells (MDA-MB-231, MCF-7, SKBR3) and non-tumorigenic breast epithelial cells (MCF-10A). ( C ) CCK-8 assay showing reduced proliferation rates in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells following isoliquiritigenin treatment. ( D , E ) Colony formation assays revealed that isoliquiritigenin significantly inhibited clonogenic potential in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells. ( F ) Transwell assays demonstrated reduced migratory capacity of MDA-MB-231 cells after isoliquiritigenin-induced PITX1 inhibition. Scale bar: 50 μm. ( G ) Glucose uptake was decreased in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells following isoliquiritigenin treatment. ( H ) Lactate production was reduced in all three cell lines upon PITX1 inhibition. ( I ) Western blot analysis revealed downregulation of PFKP protein levels in MDA-MB-231, MCF-7, SKBR3, and MCF-10A cells after isoliquiritigenin treatment. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Isoliquiritigenin (ISL) was purchased from MedChemExpress (MCE, Monmouth Junction, NJ, USA; Cat. No. HY-N0373).

Techniques: Expressing, CCK-8 Assay, Inhibition, Western Blot

Chalcone derivatives inhibited TNF-α-induced ICAM-1 expression. ( A ) Structures of 4′-hydroxychalcone, isoliquiritigenin, and xanthohumol. ( B – G ) A549 cells were treated with 4′-hydroxychalcone ( B , E ), isoliquiritigenin ( C , F ), and xanthohumol ( D , G ) for 1 h, followed by a 6-h stimulation with (+) or without (−) TNF-α (2.5 ng/mL) in the presence or absence of 4′-hydroxychalcone, isoliquiritigenin, and xanthohumol (5–50 µM). Cell viability (%) (blue bars) is presented as the mean ± standard error ( n = 3) ( B – D ). No significant differences were observed ( B – D ). ICAM-1 expression (%) (magenta bars) is presented as the mean ± standard error ( n = 3) ( E – G ). *** p < 0.001.

Journal: Molecules

Article Title: Cardamonin Inhibits the Nuclear Translocation and DNA Binding of RelA in the Tumor Necrosis Factor-α-Induced NF-κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

doi: 10.3390/molecules30224324

Figure Lengend Snippet: Chalcone derivatives inhibited TNF-α-induced ICAM-1 expression. ( A ) Structures of 4′-hydroxychalcone, isoliquiritigenin, and xanthohumol. ( B – G ) A549 cells were treated with 4′-hydroxychalcone ( B , E ), isoliquiritigenin ( C , F ), and xanthohumol ( D , G ) for 1 h, followed by a 6-h stimulation with (+) or without (−) TNF-α (2.5 ng/mL) in the presence or absence of 4′-hydroxychalcone, isoliquiritigenin, and xanthohumol (5–50 µM). Cell viability (%) (blue bars) is presented as the mean ± standard error ( n = 3) ( B – D ). No significant differences were observed ( B – D ). ICAM-1 expression (%) (magenta bars) is presented as the mean ± standard error ( n = 3) ( E – G ). *** p < 0.001.

Article Snippet: Cardamonin (Cayman Chemical, Ann Arbor, MI, USA), 4′-hydroxychalcone (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan), isoliquiritigenin (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan), and xanthohumol (Angene International Limited, London, UK) were obtained commercially.

Techniques: Expressing

4′-Hydroxychalcone and isoliquiritigenin did not affect TNF-α-induced IκBα degradation. ( A , B ) A549 cells were treated with 4′-hydroxychalcone, isoliquiritigenin, and xanthohumol for 1 h, followed by a 15-min stimulation with (+) or without (−) TNF-α (2.5 ng/mL) in the presence or absence of the compounds (each at 50 µM). Representative blots from three independent experiments are displayed ( A ). IκBα protein (%) (cyan bars) is presented as the mean ± standard error ( n = 3) ( B ). ** p < 0.01 and *** p < 0.001. Original blots are presented in .

Journal: Molecules

Article Title: Cardamonin Inhibits the Nuclear Translocation and DNA Binding of RelA in the Tumor Necrosis Factor-α-Induced NF-κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

doi: 10.3390/molecules30224324

Figure Lengend Snippet: 4′-Hydroxychalcone and isoliquiritigenin did not affect TNF-α-induced IκBα degradation. ( A , B ) A549 cells were treated with 4′-hydroxychalcone, isoliquiritigenin, and xanthohumol for 1 h, followed by a 15-min stimulation with (+) or without (−) TNF-α (2.5 ng/mL) in the presence or absence of the compounds (each at 50 µM). Representative blots from three independent experiments are displayed ( A ). IκBα protein (%) (cyan bars) is presented as the mean ± standard error ( n = 3) ( B ). ** p < 0.01 and *** p < 0.001. Original blots are presented in .

Article Snippet: Cardamonin (Cayman Chemical, Ann Arbor, MI, USA), 4′-hydroxychalcone (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan), isoliquiritigenin (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan), and xanthohumol (Angene International Limited, London, UK) were obtained commercially.

Techniques:

4′-Hydroxychalcone, isoliquiritigenin, and xanthohumol inhibited TNF-α-induced RelA nuclear translocation. ( A – I ) A549 cells were treated with 4′-hydroxychalcone ( A – C ), isoliquiritigenin ( D – F ), and xanthohumol ( G – I ) for 1 h, followed by a 30-min stimulation with (+) or without (−) TNF-α (2.5 ng/mL) in the presence or absence of the compounds (5–50 µM). Representative blots from three independent experiments are displayed ( A , D , G ). RelA protein (%) in the nucleus ( B , E , H ) and cytoplasm ( C , F , I ) (cyan bars) are presented as the mean ± standard error ( n = 3). * p < 0.05, ** p < 0.01, and *** p < 0.001. Original blots are presented in .

Journal: Molecules

Article Title: Cardamonin Inhibits the Nuclear Translocation and DNA Binding of RelA in the Tumor Necrosis Factor-α-Induced NF-κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

doi: 10.3390/molecules30224324

Figure Lengend Snippet: 4′-Hydroxychalcone, isoliquiritigenin, and xanthohumol inhibited TNF-α-induced RelA nuclear translocation. ( A – I ) A549 cells were treated with 4′-hydroxychalcone ( A – C ), isoliquiritigenin ( D – F ), and xanthohumol ( G – I ) for 1 h, followed by a 30-min stimulation with (+) or without (−) TNF-α (2.5 ng/mL) in the presence or absence of the compounds (5–50 µM). Representative blots from three independent experiments are displayed ( A , D , G ). RelA protein (%) in the nucleus ( B , E , H ) and cytoplasm ( C , F , I ) (cyan bars) are presented as the mean ± standard error ( n = 3). * p < 0.05, ** p < 0.01, and *** p < 0.001. Original blots are presented in .

Article Snippet: Cardamonin (Cayman Chemical, Ann Arbor, MI, USA), 4′-hydroxychalcone (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan), isoliquiritigenin (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan), and xanthohumol (Angene International Limited, London, UK) were obtained commercially.

Techniques: Translocation Assay