Objective:To summarize clinical experience of Professor QIAO Bao-zhang in treatment for pancreatic cancer,and to provide reference for clinicians.Methods:Through learning from Professor QIAO during his clinical practi...Objective:To summarize clinical experience of Professor QIAO Bao-zhang in treatment for pancreatic cancer,and to provide reference for clinicians.Methods:Through learning from Professor QIAO during his clinical practice and listening to his lectures,Professor QIAO Bao-zhang's clinically proved cases of treating pancreatic cancer based on syndrome differentiation were organized and summarized.From aspects like etiology,pathogenesis,treatment principles and treatment methods of pancreatic cancer,Professor QIAO's experience in diagnosis and treatment for this disease was analyzed and explored,and characteristics of medication were summarized.Two typical cases were selected as proof,and his treatment ideas and methods were explored.Results:Professor QIAO believes that the pathogenesis is mostly deficiency of vital Qi(正气),and stagnation of phlegm,heat and dampness in Zang-Fu(脏腑)and meridians.Around intermingled deficiency and excess,syndrome differentiation and treatment were performed.Due to treatment methods such as strengthening vital Qi to eliminate pathogenic factor,clearing heat,eliminating dampness and resolving phlegm,as well as removing toxicity and resolving hard mass,progress of malignant tumors was inhibited and recurrence and metastasis of malignant tumors were delayed.Conclusion:Professor QIAO's experience in treating pancreatic cancer is worth learning.展开更多
Objective: To determine whether monotropein has an anticancer effect and explore its potential mechanisms against colorectal cancer(CRC) through network pharmacology and molecular docking combined with experimental ve...Objective: To determine whether monotropein has an anticancer effect and explore its potential mechanisms against colorectal cancer(CRC) through network pharmacology and molecular docking combined with experimental verification. Methods: Network pharmacology and molecular docking were used to predict potential targets of monotropein against CRC. Cell counting kit assay, plate monoclonal assay and microscopic observation were used to investigate the antiproliferative effects of monotropein on CRC cells HCT116, HT29 and LoVo. Flow cytometry and scratch assay were used to analyze apoptosis and cell cycle, as well as cell migration, respectively in HCT116, HT29, and LoVo cells. Western blotting was used to detect the expression of proteins related to apoptosis, cell cycle, and cell migration, and the expression of proteins key to the Akt pathway. Results: The Gene Ontology and Reactome enrichment analyses indicated that the anticancer potential of monotropein against CRC might be involved in multiple cancer-related signaling pathways. Among these pathways, RAC-beta serine/threonine-protein kinase(Akt1, Akt2), cyclin-dependent kinase 6(CDK6), matrix metalloproteinase-9(MMP9), epidermal growth factor receptor(EGFR), cell division control protein 42 homolog(CDC42) were shown as the potential anticancer targets of monotropein against CRC. Molecular docking suggested that monotropein may interact with the 6 targets(Akt1, Akt2, CDK6, MMP9, EGFR, CDC42). Subsequently, cell activity of HCT116, HT29 and LoVo cell lines were significantly suppressed by monotropein(P<0.05). Furthermore, our research revealed that monotropein induced cell apoptosis by inhibiting Bcl-2 and increasing Bax, induced G_1–S cycle arrest in colorectal cancer by decreasing the expressions of CyclinD1, CDK4 and CDK6, inhibited cell migration by suppressing the expressions of CDC42 and MMP9(P<0.05), and might play an anticancer role through Akt signaling pathway. Conclusions: Monotropein exerts its antitumor effects primarily by arresting the cell cycle, causing cell apoptosis, and inhibiting cell migration. This indicates a high potential for developing novel medication for treating CRC.展开更多
基金Science and Technology Coordination and Innovation Projects of Shaanxi Province(2016KTCL03-16)。
文摘Objective:To summarize clinical experience of Professor QIAO Bao-zhang in treatment for pancreatic cancer,and to provide reference for clinicians.Methods:Through learning from Professor QIAO during his clinical practice and listening to his lectures,Professor QIAO Bao-zhang's clinically proved cases of treating pancreatic cancer based on syndrome differentiation were organized and summarized.From aspects like etiology,pathogenesis,treatment principles and treatment methods of pancreatic cancer,Professor QIAO's experience in diagnosis and treatment for this disease was analyzed and explored,and characteristics of medication were summarized.Two typical cases were selected as proof,and his treatment ideas and methods were explored.Results:Professor QIAO believes that the pathogenesis is mostly deficiency of vital Qi(正气),and stagnation of phlegm,heat and dampness in Zang-Fu(脏腑)and meridians.Around intermingled deficiency and excess,syndrome differentiation and treatment were performed.Due to treatment methods such as strengthening vital Qi to eliminate pathogenic factor,clearing heat,eliminating dampness and resolving phlegm,as well as removing toxicity and resolving hard mass,progress of malignant tumors was inhibited and recurrence and metastasis of malignant tumors were delayed.Conclusion:Professor QIAO's experience in treating pancreatic cancer is worth learning.
文摘Objective: To determine whether monotropein has an anticancer effect and explore its potential mechanisms against colorectal cancer(CRC) through network pharmacology and molecular docking combined with experimental verification. Methods: Network pharmacology and molecular docking were used to predict potential targets of monotropein against CRC. Cell counting kit assay, plate monoclonal assay and microscopic observation were used to investigate the antiproliferative effects of monotropein on CRC cells HCT116, HT29 and LoVo. Flow cytometry and scratch assay were used to analyze apoptosis and cell cycle, as well as cell migration, respectively in HCT116, HT29, and LoVo cells. Western blotting was used to detect the expression of proteins related to apoptosis, cell cycle, and cell migration, and the expression of proteins key to the Akt pathway. Results: The Gene Ontology and Reactome enrichment analyses indicated that the anticancer potential of monotropein against CRC might be involved in multiple cancer-related signaling pathways. Among these pathways, RAC-beta serine/threonine-protein kinase(Akt1, Akt2), cyclin-dependent kinase 6(CDK6), matrix metalloproteinase-9(MMP9), epidermal growth factor receptor(EGFR), cell division control protein 42 homolog(CDC42) were shown as the potential anticancer targets of monotropein against CRC. Molecular docking suggested that monotropein may interact with the 6 targets(Akt1, Akt2, CDK6, MMP9, EGFR, CDC42). Subsequently, cell activity of HCT116, HT29 and LoVo cell lines were significantly suppressed by monotropein(P<0.05). Furthermore, our research revealed that monotropein induced cell apoptosis by inhibiting Bcl-2 and increasing Bax, induced G_1–S cycle arrest in colorectal cancer by decreasing the expressions of CyclinD1, CDK4 and CDK6, inhibited cell migration by suppressing the expressions of CDC42 and MMP9(P<0.05), and might play an anticancer role through Akt signaling pathway. Conclusions: Monotropein exerts its antitumor effects primarily by arresting the cell cycle, causing cell apoptosis, and inhibiting cell migration. This indicates a high potential for developing novel medication for treating CRC.
