Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liriodenine has wide pharmacological functions in phytochemistry, pharmacology and antitumor activities. The anticancer effects of liriodenine on the cell growth and apoptosis of human breast cancer MCF-7 cells, and the underlying mechanisms, are yet to be elucidated. Therefore, the present study investigated the anticancer effects of liriodenine on the cell growth and apoptosis of human breast cancer MCF-7 cells. We used MTT assay to measure cell growth, and flow cytometer and DAPI staining was used to analyze cell apoptosis. Then, Western blot analysis was executed to measure B-cell lymphoma-2 protein (Bcl-2), cyclin D1, vascular endothelial growth factor (VEGF), and p53 protein expression. The effect of liriodenine induced significant apoptosis and suppression of cell growth of the MCF-7 cells. Furthermore, the potential mechanism underlying its antitumor effect on MCF-7 cells may result from activation of caspase-3 activity, Bcl-2, cyclin D1 and VEGF, and promotion of p53 protein expression in MCF-7 cells. Therefore, the present results indicated that the anticancer effects of liriodenine suppress cell growth and induce the apoptosis of human breast cancer MCF-7 cells through inhibition of Bcl-2, cyclin D1 and VEGF expression, and upregulation of p53 expression. Therefore, liriodenine may be a potential therapy for the treatment of human breast cancer.
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PMID:Anticancer effects of liriodenine on the cell growth and apoptosis of human breast cancer MCF-7 cells through the upregulation of p53 expression. 2878 41

At present, chemotherapy and radiotherapy represent the primary modalities of treatment for patients with unresectable esophageal squamous cell carcinoma (ESCC). However, the outcome of patients remains poor owing to radioresistance. The present study aimed to determine the radiosensitizing effect of liriodenine, an aporphine alkaloid derived from Enicosanthellum pulchrum, and investigating the underlying mechanisms in ESCC, using the esophageal cancer ECA-109 cell line. Cellular proliferation was evaluated using the Cell Counting kit-8 assay. Colony formation assay was performed to characterize the radiosensitive effects of liriodenine on ECA-109 cells, and flow cytometry was used to detect the percentage of cells undergoing apoptosis. An immunofluorescence assay was utilized to evaluate the DNA damage repair ability. Western blotting was used to assess the protein levels of caspase-3, B cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax). Liriodenine dose-dependently inhibited ECA-109 cell viability. The clonogenic survival assay demonstrated that liriodenine increased the radiosensitivity of ESCC cells, with a sensitization enhancement ratio of 1.11-1.69. The results of flow cytometry demonstrated that liriodenine induced apoptosis and G2/M arrest. The immunofluorescence assay revealed that liriodenine delays DNA damage repair. The upregulation of Bax and Caspase-3, and the suppression of Bcl-2 confirmed that apoptosis was occurring. Liriodenine radiosensitizes ECA-109 cells by inducing apoptosis and G2/M arrest. The findings of the present study indicated that liriodenine may represent an anticancer agent with promising potential for the treatment of ESCC.
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PMID:Liriodenine enhances radiosensitivity in esophageal cancer ECA-109 cells by inducing apoptosis and G2/M arrest. 3025 May 68