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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, BH3 interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.

Journal: Translational Cancer Research

Article Title: Neochlorogenic acid inhibits gastric cancer cell growth through apoptosis and cell cycle arrest

doi: 10.21037/tcr-2025-696

Figure Lengend Snippet: Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, BH3 interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.

Article Snippet: The membranes were then incubated overnight at 4 °C with primary antibodies for BCL2 (B-cell lymphoma 2) (Cat. No. bs-0032R; Bioss, Beijing, China), BID (BH3 interacting domain death agonist) (Cat. No. 10988-1-AP), CYCS (cytochrome c, somatic) (Cat. No. 10993-1-AP) from Proteintech (Wuhan, China), as well as β-actin (Cat. No. 81115-1-RR, Proteintech, Wuhan, China) and BAX (BCL2-associated X protein) (Cat. No. 50599-2-Ig, Proteintech, Wuhan, China).

Techniques: Western Blot, Control, Expressing, Standard Deviation