Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (1): 149-159.DOI: 10.19852/j.cnki.jtcm.2026.01.014
• Original Articles • Previous Articles Next Articles
Mechanisms of Gualou Beimu Yin (瓜蒌贝母饮) in suppressing the development and metastasis of triple-negative breast cancer: an integrated study based on network pharmacology, transcriptomics, and metabolomics
JIA Ao1, LIU Shuang1, GAO Tingting1, ZHANG Haoran1, GAO Wenyuan2(
), WU Xiongzhi3()
- 1 Tianjin NanKai Hospital, Tianjin Medical University, Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Institute of Integrative Medicine for Acute Abdominal Diseases, Tianjin 300000, China
2 School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 300000, China
3 Tianjin NanKai Hospital, Tianjin Medical University, Tianjin 300000, China
-
Received:2024-10-26Accepted:2025-02-22Online:2026-02-15Published:2026-01-28 -
Contact:Prof. WU Xiongzhi, Tianjin NanKai Hospital, Tianjin Medical University, Tianjin 300000, China.wuxiongzhi@163.com ; Prof. GAO Wenyuan, School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 300000, China.pharmgao@tju.edu.cn ;Telephone: +86-22-27435890 -
About author:JIA Ao andLIU Shuang are co-first authors and contributed equally to this work -
Supported by:National Natural Science Foundation of China: Study on Mechanism of Transdifferentiation of Hepatocellular Carcinoma Cells Induced by Huoxue Ruanjian Traditional Chinese Medicine(82174103)
Cite this article
JIA Ao, LIU Shuang, GAO Tingting, ZHANG Haoran, GAO Wenyuan, WU Xiongzhi. Mechanisms of Gualou Beimu Yin (瓜蒌贝母饮) in suppressing the development and metastasis of triple-negative breast cancer: an integrated study based on network pharmacology, transcriptomics, and metabolomics[J]. Journal of Traditional Chinese Medicine, 2026, 46(1): 149-159.
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Figure 1 Cell experiments demonstrating that GLBMY has an inhibitory effect on TNBC A: wound healing assay showing the migratory ability of MDA-MB-231 cells under different GLBMY concentrations (n = 4, × 200, scale bar = 100 μm); B: wound healing assay showing the migratory ability of BT549 cells under different GLBMY concentrations (n = 4, × 200, scale bar = 100 μm); C: Western blot analysis of BCL2, BAX protein expression in MDA-MB-231 cells (n = 4); D: Western blot analysis of RIPK3, MLKL and P-MLKL protein expression in MDA-MB-231 cells (n = 4); E: Western blot analysis of BCL2, BAX protein expression in BT549 cells (n = 4); F: Western blot analysis of RIPK3, MLKL and P-MLKL protein expression in BT549 cells (n = 4). A1, A4, A7, A10, B1, B4, B7, B10: 0 h; A2, A5, A8, A11, B2, B5, B8, B11: 24 h; A3, A6, A9, A12, B3, B6, B9, B12: 48 h; A1, A2, A3, B1, B2, B3: Negative Control group; A4, A5, A6, B4, B5, B6: GLBMY (75 μg/mL ) group; A7, A8, A9, B7, B8, B9: GLBMY (150 μg/mL ) group; A10, A11, A12, B10, B11, B12: GLBMY (250 μg/mL ) group. C-F: cells were treated with lyophilized GLBMY powder dissolved in complete DMEM at final concentrations of 0, 75, 150, and 250 μg/mL for 24 h. The control group received vehicle only (0 μg/mL GLBMY). GLBMY: Gualou Beimu Yin; β-actin: beta-actin; BCL-2: b-cell lymphoma 2; BAX: bcl-2-associated x protein; RIPK3: receptor-interacting serine/threonine-protein kinase 3; MLKL: mixed lineage kinase domain-like protein; p-MLKL: phosphorylated mixed lineage kinase domain-like protein.
Figure 1 Cell experiments demonstrating that GLBMY has an inhibitory effect on TNBC A: wound healing assay showing the migratory ability of MDA-MB-231 cells under different GLBMY concentrations (n = 4, × 200, scale bar = 100 μm); B: wound healing assay showing the migratory ability of BT549 cells under different GLBMY concentrations (n = 4, × 200, scale bar = 100 μm); C: Western blot analysis of BCL2, BAX protein expression in MDA-MB-231 cells (n = 4); D: Western blot analysis of RIPK3, MLKL and P-MLKL protein expression in MDA-MB-231 cells (n = 4); E: Western blot analysis of BCL2, BAX protein expression in BT549 cells (n = 4); F: Western blot analysis of RIPK3, MLKL and P-MLKL protein expression in BT549 cells (n = 4). A1, A4, A7, A10, B1, B4, B7, B10: 0 h; A2, A5, A8, A11, B2, B5, B8, B11: 24 h; A3, A6, A9, A12, B3, B6, B9, B12: 48 h; A1, A2, A3, B1, B2, B3: Negative Control group; A4, A5, A6, B4, B5, B6: GLBMY (75 μg/mL ) group; A7, A8, A9, B7, B8, B9: GLBMY (150 μg/mL ) group; A10, A11, A12, B10, B11, B12: GLBMY (250 μg/mL ) group. C-F: cells were treated with lyophilized GLBMY powder dissolved in complete DMEM at final concentrations of 0, 75, 150, and 250 μg/mL for 24 h. The control group received vehicle only (0 μg/mL GLBMY). GLBMY: Gualou Beimu Yin; β-actin: beta-actin; BCL-2: b-cell lymphoma 2; BAX: bcl-2-associated x protein; RIPK3: receptor-interacting serine/threonine-protein kinase 3; MLKL: mixed lineage kinase domain-like protein; p-MLKL: phosphorylated mixed lineage kinase domain-like protein.
Figure 2 GLBMY suppresses TNBC tumor growth and lung metastasis in vivo A: representative images of tumors excised from mice in each treatment group (n = 6); B: representative images of lung metastases in each treatment group; C: HE staining of lung tissues (× 50, scale bar = 100 μm); D: Western blot analysis of BCL2, BAX protein expression in tumor tissues from mice treated with GLBMY and cisplatin (n = 4); E: Western blot analysis of RIPK3, MLKL, and P-MLKL protein expression in tumor tissues from mice treated with GLBMY and cisplatin (n = 4); F: Western blot analysis of MMP9, E-CAD, α-SMA, and VIM protein expression in tumor tissues treated with GLBMY and cisplatin (n = 4). A1, B1, C1: Negative Control group; A2, B2, C2: GLBMY-L (6.43 g·kg?1·d?1) group; A3, B3, C3: GLBMY-H (12.86 g·kg?1·d?1) group; A4, B4, C4: cisplatin (2 mg/kg every 3 d) group; A5, B5, C5: Cisplatin + GLBMY (H) group. NC group: mice received vehicle by oral gavage once daily throughout the experimental period; GLBMY-L group: mice were orally administered Gualou Beimu Yin (GLBMY) at a dose of 6.43 g·kg?1·d?1 by gavage once daily throughout the treatment period; GLBMY-H group: mice were orally administered GLBMY at a dose of 12.86 g·kg?1·d?1 by gavage once daily throughout the treatment period; Cisplatin group: mice received cisplatin (2 mg/kg) by intraperitoneal injection once every 3 d throughout the treatment period; Cisplatin + GLBMY-H group: mice were treated with cisplatin (2 mg/kg, intraperitoneally once every 3 d) in combination with GLBMY (12.86 g·kg?1·d?1, orally once daily) throughout the experimental period. NC: negative control; GLBMY: Gualou Beimu Yin; β-actin: beta-actin; BCL-2: b-cell lymphoma 2; BAX: bcl-2-associated x protein; RIPK3: receptor-interacting serine/threonine-protein kinase 3; MLKL: mixed lineage kinase domain-like protein; p-MLKL: phosphorylated mixed lineage kinase domain-like protein; MMP9: matrix metalloproteinase-9; α-SMA: alpha-smooth muscle actin; E-CAD: e-cadherin; VIM: vimentin.
Figure 2 GLBMY suppresses TNBC tumor growth and lung metastasis in vivo A: representative images of tumors excised from mice in each treatment group (n = 6); B: representative images of lung metastases in each treatment group; C: HE staining of lung tissues (× 50, scale bar = 100 μm); D: Western blot analysis of BCL2, BAX protein expression in tumor tissues from mice treated with GLBMY and cisplatin (n = 4); E: Western blot analysis of RIPK3, MLKL, and P-MLKL protein expression in tumor tissues from mice treated with GLBMY and cisplatin (n = 4); F: Western blot analysis of MMP9, E-CAD, α-SMA, and VIM protein expression in tumor tissues treated with GLBMY and cisplatin (n = 4). A1, B1, C1: Negative Control group; A2, B2, C2: GLBMY-L (6.43 g·kg?1·d?1) group; A3, B3, C3: GLBMY-H (12.86 g·kg?1·d?1) group; A4, B4, C4: cisplatin (2 mg/kg every 3 d) group; A5, B5, C5: Cisplatin + GLBMY (H) group. NC group: mice received vehicle by oral gavage once daily throughout the experimental period; GLBMY-L group: mice were orally administered Gualou Beimu Yin (GLBMY) at a dose of 6.43 g·kg?1·d?1 by gavage once daily throughout the treatment period; GLBMY-H group: mice were orally administered GLBMY at a dose of 12.86 g·kg?1·d?1 by gavage once daily throughout the treatment period; Cisplatin group: mice received cisplatin (2 mg/kg) by intraperitoneal injection once every 3 d throughout the treatment period; Cisplatin + GLBMY-H group: mice were treated with cisplatin (2 mg/kg, intraperitoneally once every 3 d) in combination with GLBMY (12.86 g·kg?1·d?1, orally once daily) throughout the experimental period. NC: negative control; GLBMY: Gualou Beimu Yin; β-actin: beta-actin; BCL-2: b-cell lymphoma 2; BAX: bcl-2-associated x protein; RIPK3: receptor-interacting serine/threonine-protein kinase 3; MLKL: mixed lineage kinase domain-like protein; p-MLKL: phosphorylated mixed lineage kinase domain-like protein; MMP9: matrix metalloproteinase-9; α-SMA: alpha-smooth muscle actin; E-CAD: e-cadherin; VIM: vimentin.
Figure 3 Multi-omics analysis reveals the molecular mechanisms underlying the antitumor effects of GLBMY A: KEGG pathway enrichment analyses in Network pharmacology; B: molecular docking of selected active ingredients with target proteins; C: KEGG pathway enrichment analyses in RNA-seq; D: VIP statistics of key differentially abundant metabolites; E: MetPA enrichment analysis. B1: tubeimoside I-Il6; B2: tubeimoside I-MAPK3; B3: tubeimoside I-STAT3. GLBMY: Gualou Beimu Yin; KEGG: kyoto encyclopedia of genes and genomes; VIP: variable importance in projection; MetPA: metabolomics pathway analysis; PI3K: phosphoinositide 3-kinase; Akt: protein kinase b; AGE: advanced glycation end-products; RAGE: receptor for advanced glycation end-products; NF-kappa B: nuclear factor kappa-light-chain-enhancer of activated b cells; Ras: rat sarcoma virus oncogene; Wnt: wingless-related integration site; Rap1: ras-proximate-1; MAPK: mitogen-activated protein kinase; VEGF: vascular endothelial growth factor; JAK: janus kinase; STAT: signal transducer and activator of transcription; CGMP: cyclic guanosine monophosphate; PKG: protein kinase g; CAMP: cyclic adenosine monophosphate; MTOR: mechanistic target of rapamycin; HIF-1: hypoxia-inducible factor 1; FoxO: forkhead box o; ErbB: erythroblastic leukemia viral oncogene homolog; TGF-beta: transforming growth factor beta; TNF: tumor necrosis factor; dTMP: deoxythymidine monophosphate; TCA cycle: tricarboxylic acid cycle; CoA: coenzyme A.
Figure 3 Multi-omics analysis reveals the molecular mechanisms underlying the antitumor effects of GLBMY A: KEGG pathway enrichment analyses in Network pharmacology; B: molecular docking of selected active ingredients with target proteins; C: KEGG pathway enrichment analyses in RNA-seq; D: VIP statistics of key differentially abundant metabolites; E: MetPA enrichment analysis. B1: tubeimoside I-Il6; B2: tubeimoside I-MAPK3; B3: tubeimoside I-STAT3. GLBMY: Gualou Beimu Yin; KEGG: kyoto encyclopedia of genes and genomes; VIP: variable importance in projection; MetPA: metabolomics pathway analysis; PI3K: phosphoinositide 3-kinase; Akt: protein kinase b; AGE: advanced glycation end-products; RAGE: receptor for advanced glycation end-products; NF-kappa B: nuclear factor kappa-light-chain-enhancer of activated b cells; Ras: rat sarcoma virus oncogene; Wnt: wingless-related integration site; Rap1: ras-proximate-1; MAPK: mitogen-activated protein kinase; VEGF: vascular endothelial growth factor; JAK: janus kinase; STAT: signal transducer and activator of transcription; CGMP: cyclic guanosine monophosphate; PKG: protein kinase g; CAMP: cyclic adenosine monophosphate; MTOR: mechanistic target of rapamycin; HIF-1: hypoxia-inducible factor 1; FoxO: forkhead box o; ErbB: erythroblastic leukemia viral oncogene homolog; TGF-beta: transforming growth factor beta; TNF: tumor necrosis factor; dTMP: deoxythymidine monophosphate; TCA cycle: tricarboxylic acid cycle; CoA: coenzyme A.
Figure 4 Integrated multi-omics analysis identifies key signaling pathways and validates GLBMY-regulated genes A: expression profiles of DEGs in MAPK/ERK pathway identified through network pharmacology and RNA-seq; B: expression profiles of DEGs in IL6-STAT pathway identified through network pharmacology and RNA-seq; C: Western blot analysis of MAPK/ERK pathway proteins in MDA-MB-231 cells (n = 4); D: Western blot analysis of MAPK/ERK pathway proteins in BT549 cells (n = 4); E: Western blot analysis of MAPK/ERK pathway proteins in vivo (n = 4); F: Western blot analysis of IL6-STAT pathway proteins in MDA-MB-231 cells (n = 4); G: Western blot analysis of IL6-STAT pathway proteins in BT549 cells (n = 4); H: Western blot analysis of IL6-STAT pathway proteins in vivo (n = 4). Cells were treated with lyophilized GLBMY powder dissolved in complete DMEM at final concentrations of 0, 75, 150, and 250 μg/mL for 24 h. The control group received vehicle only (0 μg/mL GLBMY). NC group: mice received vehicle by oral gavage once daily throughout the experimental period; GLBMY-L group: mice were orally administered Gualou Beimu Yin (GLBMY) at a dose of 6.43 g·kg?1·d?1 by gavage once daily throughout the treatment period; GLBMY-H group: mice were orally administered GLBMY at a dose of 12.86 g·kg?1·d?1 by gavage once daily throughout the treatment period; Cisplatin group: mice received cisplatin (2 mg/kg) by intraperitoneal injection once every 3 d throughout the treatment period; Cisplatin + GLBMY-H group: mice were treated with cisplatin (2 mg/kg, intraperitoneally once every 3 d) in combination with GLBMY (12.86 g·kg?1·d?1, orally once daily) throughout the experimental period. DEGs: differentially expressed genes; MAPK/ERK: mitogen-activated protein kinase/extracellular signal-regulated kinase; Ntrk1: neurotrophic tyrosine kinase receptor type 1; Rasgrp1: ras guanyl releasing protein 1; Rasgrp2: ras guanyl releasing protein 2; Cacna1i: calcium voltage-gated channel subunit alpha1 i; Prkcb: protein kinase c beta; Cntfr: ciliary neurotrophic factor receptor; Il9r: interleukin 9 receptor; Il22ra2: interleukin 22 receptor subunit alpha 2; Gfap: glial fibrillary acidic protein; Il27ra: interleukin 27 receptor subunit alpha; NC: negative control; GLBMY: Gualou Beimu Yin; β-actin: beta-actin; ERK1/2: extracellular signal-regulated kinase 1/2; p-ERK1/2: phosphorylated extracellular signal-regulated kinase 1/2; IL6: interleukin-6; STAT3: signal transducer and activator of transcription 3; p-STAT3: phosphorylated signal transducer and activator of transcription 3. The 2-△△CT method was used to analyse relative gene expression. Data are presented as mean ± standard deviation. Two-group comparisons used Student’s t-test. Compared with the Negative Control group, aP < 0.05.
Figure 4 Integrated multi-omics analysis identifies key signaling pathways and validates GLBMY-regulated genes A: expression profiles of DEGs in MAPK/ERK pathway identified through network pharmacology and RNA-seq; B: expression profiles of DEGs in IL6-STAT pathway identified through network pharmacology and RNA-seq; C: Western blot analysis of MAPK/ERK pathway proteins in MDA-MB-231 cells (n = 4); D: Western blot analysis of MAPK/ERK pathway proteins in BT549 cells (n = 4); E: Western blot analysis of MAPK/ERK pathway proteins in vivo (n = 4); F: Western blot analysis of IL6-STAT pathway proteins in MDA-MB-231 cells (n = 4); G: Western blot analysis of IL6-STAT pathway proteins in BT549 cells (n = 4); H: Western blot analysis of IL6-STAT pathway proteins in vivo (n = 4). Cells were treated with lyophilized GLBMY powder dissolved in complete DMEM at final concentrations of 0, 75, 150, and 250 μg/mL for 24 h. The control group received vehicle only (0 μg/mL GLBMY). NC group: mice received vehicle by oral gavage once daily throughout the experimental period; GLBMY-L group: mice were orally administered Gualou Beimu Yin (GLBMY) at a dose of 6.43 g·kg?1·d?1 by gavage once daily throughout the treatment period; GLBMY-H group: mice were orally administered GLBMY at a dose of 12.86 g·kg?1·d?1 by gavage once daily throughout the treatment period; Cisplatin group: mice received cisplatin (2 mg/kg) by intraperitoneal injection once every 3 d throughout the treatment period; Cisplatin + GLBMY-H group: mice were treated with cisplatin (2 mg/kg, intraperitoneally once every 3 d) in combination with GLBMY (12.86 g·kg?1·d?1, orally once daily) throughout the experimental period. DEGs: differentially expressed genes; MAPK/ERK: mitogen-activated protein kinase/extracellular signal-regulated kinase; Ntrk1: neurotrophic tyrosine kinase receptor type 1; Rasgrp1: ras guanyl releasing protein 1; Rasgrp2: ras guanyl releasing protein 2; Cacna1i: calcium voltage-gated channel subunit alpha1 i; Prkcb: protein kinase c beta; Cntfr: ciliary neurotrophic factor receptor; Il9r: interleukin 9 receptor; Il22ra2: interleukin 22 receptor subunit alpha 2; Gfap: glial fibrillary acidic protein; Il27ra: interleukin 27 receptor subunit alpha; NC: negative control; GLBMY: Gualou Beimu Yin; β-actin: beta-actin; ERK1/2: extracellular signal-regulated kinase 1/2; p-ERK1/2: phosphorylated extracellular signal-regulated kinase 1/2; IL6: interleukin-6; STAT3: signal transducer and activator of transcription 3; p-STAT3: phosphorylated signal transducer and activator of transcription 3. The 2-△△CT method was used to analyse relative gene expression. Data are presented as mean ± standard deviation. Two-group comparisons used Student’s t-test. Compared with the Negative Control group, aP < 0.05.
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