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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
Her2, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
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fibroblast growth factor 2  (R&D Systems)
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
E El H1603, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
Human Growth Factor Profiling, supplied by RayBiotech inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
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fibroblast growth factor 2 g3 fgf2 g3  (Qkine Ltd)
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
Fibroblast Growth Factor 2 G3 Fgf2 G3, supplied by Qkine Ltd, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
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nerve growth factor ngf  (Alomone Labs)
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assay</t> <t>(ELISA)</t> in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.
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Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by enzyme‐linked immunosorbent assay (ELISA) in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.

Journal: Advanced Science

Article Title: Lactylation‐Mediated HER2 Stabilization Promotes Trastuzumab Resistance in Gastric Cancer

doi: 10.1002/advs.77955

Figure Lengend Snippet: Lactate promotes trastuzumab resistance in gastric cancer by stabilizing HER2 expression. (a) Volcano plot illustrating metabolic differences between gastric cancer tissues from patients who subsequently developed trastuzumab resistance ( n = 6) and those who remained trastuzumab‐sensitive ( n = 6), as determined by untargeted metabolomics analysis. All tissues were surgically resected prior to trastuzumab treatment, and sensitivity or resistance to trastuzumab was subsequently determined based on clinical pathology data and patient follow‐up information. Red dots represent metabolites involved in the glycolytic pathway. (b) Lactate levels in gastric cancer specimens measured using a colorimetric assay kit (all samples assayed in duplicate). Each patient sample is shown in a distinct color, and the two technical replicates from the same patient are shown in the same color. (c) HER2 protein levels measured by enzyme‐linked immunosorbent assay (ELISA) in gastric cancer samples (LAC low , n = 6; LAC High , n = 6). (d,e) HER2 protein levels in AGS cells following treatment with sodium lactate (NALA, 25 or 50 m m ) and lactate (10 or 20 m m ). (f,g) HER2 protein levels in AGS cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (h,i) HER2 protein levels in NCI‐N87 cells following treatment with NALA (25 or 50 m m ) and lactate (10 or 20 m m ). (j,k) HER2 protein levels in NCI‐N87 cells following treatment with sodium oxamate (10 or 20 m m ) and stiripentol (100 or 200 µ m ). (l) Flow cytometric analysis of HER2 protein expression in AGS cells treated with NALA or lactate dehydrogenase inhibitors (LDHi) ( n = 3). (m) Flow cytometric analysis of HER2 protein expression in NCI‐N87 cells treated with NALA or LDHi ( n = 3). (n) Representative immunofluorescence (IF) staining and co‐localization analysis of pan‐lactylation and HER2 in gastric cancer tissues (scale bars, 20 µm). (o) Correlation between pan‐lactylation and HER2 expression in gastric cancer tissues (Spearman correlation analysis). (p,q) Lactylation levels of exogenous and endogenous HER2 in cells treated with NALA or LDHi. (r,s) HER2 protein levels in 293T and NCI‐N87 cells treated with LDHi and/or MG132 (10 µ m ). (t,u) Ubiquitination of exogenous and endogenous HER2 following NALA treatment. (v,w) Ubiquitination of exogenous and endogenous HER2 following LDHi treatment. p ‐values were determined by Student's t ‐test; ns, not significant. Data are presented as mean ± SD.

Article Snippet: The concentration of HER2 was measured using a commercial ELISA kit (Elabscience E‐EL‐H6083) according to the product's instructions.

Techniques: Expressing, Analysis, Sensitivity, Pathology, Colorimetric Assay, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Ubiquitin Proteomics