Dracorhodin perchlorate induces apoptosis in bladder cancer cells through Bcl-2, Bcl-XL, survivin down-regulation and caspase-3 activation

Wei, Wei; Di, Jun; Rasul, Azhar; Zhao, Chaoyue; Millimouno, Faya Martin; Tsuji, Ichiro; Iqal, Furhan; Malhi, Mahadev; Li, Yongming; Jiang, Li

doi:10.3329/bjp.v8i3.15025

Cited by 2 publications

(2 citation statements)

References 29 publications

(44 reference statements)

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“…Bladder cancer is a heterogeneous tumor with a high incidence in men and is the fourth leading cause of death from cancer in men. Studies have confirmed that heavy drinking and smoking are risk factors for bladder cancer [9] . The choice of treatment depends on the tumor pathological grade and stage, primary tumor resection or combined with bladder perfusion of chemotherapy drugs were mainly used for early non-muscular infiltrating bladder cancer, while radical cystectomy was mainly used for muscular infiltrating bladder cancer and the prognosis of patients was significantly improved with the combined application of neoadjuvant systemic chemotherapy and radiotherapy [10] .…”

Section: Resultsmentioning

confidence: 91%

Effect the Mechanism of Emodin Combined with Cp-1 on Proliferation and Apoptosis of Bladder Cancer Cell Line BIU-87

Yu¹,

Yang²

2021

ijps

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To investigate the effect of emodin combined with Cp-1 on the proliferation and apoptosis of bladder cancer cell line BIU-87. BIU-87 cells were randomly divided into control group, Cp-1 group, emodin group, Cp-1 combined with emodin group. Flow cytometry was used to detect the apoptosis of BIU-87 cells. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay was used to detect the proliferation of BIU-87 cells. Western blot and reverse transcription-polymerase chain reaction were used to detect the recepteur d'origine nantais, Caspase-3 and B-cell lymphoma 2 expressions. Compared with control group, the cell survival rate of Cp-1 group, emodin group and Cp-1 combined with emodin groupwas significantly decreased, especially in Cp-1 combined with emodin group, which was significantly lower than that of Cp-1 group and emodin group (p<0.05), while the cell apoptosis rate of Cp-1 group, emodin group and Cp-1 combined with emodin group was significantly increased, especially in Cp-1 combined with emodin group, which was significantly higher than that of Cp-1 group and emodin group (p<0.05) and the expression of recepteur d'origine nantais decreased significantly (p<0.05). Inhibition of recepteur d'origine nantais expression suppressed B-cell lymphoma 2 and increased Caspase-3 significantly (p<0.05). Our results indicated that emodin combined with Cp-1 could enhance the apoptosis and inhibit proliferation of bladder cancer cells. The mechanism may be that emodin can inhibit the expression of recepteur d'origine nantais, down regulated the expression of B-cell lymphoma 2, which increased the expression of caspase-3 in bladder cancer cells and promoted the apoptosis of bladder cancer cells.

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Section: Resultsmentioning

confidence: 91%

Effect the Mechanism of Emodin Combined with Cp-1 on Proliferation and Apoptosis of Bladder Cancer Cell Line BIU-87

Yu¹,

Yang²

2021

ijps

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“…Flow cytometric analysis was carried out immediately after the staining. Cell Quest software was utilized for sample data acquisition and subsequent analysis [ 38 ].…”

Section: Methodsmentioning

confidence: 99%

Identification of Lignan Compounds as New 6-Phosphogluconate Dehydrogenase Inhibitors for Lung Cancer

et al. 2022

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Targeting pentose phosphate pathway (PPP) enzymes has emerged as a promising strategy to combat cancer. 6-Phosphogluconate dehydrogenase (6-PGD), the third critical enzyme of the PPP, catalyzes oxidative decarboxylation of 6-phosphogluconate (6-PG) to produce ribulose-5-phosphate (Ru-5-P) and CO2. Overexpression of 6-PGD has been reported in multiple cancers and is recognized as a potential anticancer drug target. The current study is focused on the utilization of indispensable virtual screening tools for structure-based drug discovery. During the study, 17,000 natural compounds were screened against the 3-phosphoglycerate (3-PG) binding site of 6-PGD through a molecular operating environment (MOE), which revealed 115 inhibitors with higher selectivity and binding affinity. Out of the 115 best-fit compounds within the 6-PGD binding cavity, 15 compounds were selected and optimized through stringent in silico ADMET assessment models that justified the desirable pharmacokinetic, pharmacodynamic and physicochemical profiles of 5 ligands. Further protein–ligand stability assessment through molecular dynamics (MD) simulation illustrated three potential hits, secoisolariciresinol, syringaresinol and cleomiscosin A, with stable confirmation. Moreover, 6-PGD inhibitor validation was performed by an in vitro enzymatic assay using human erythrocytes purified 6-PGD protein and A549 cell lysate protein. The results of the in vitro assays supported the in silico findings. In order to gain insight into the anticancer activity of the aforementioned compounds, they were subjected to CLC-Pred, an in silico cytotoxicity browsing tool, which proved their anticancer activity against several cancer cell lines at Pa > 0.5. Additionally, a confirmation for in silico cytotoxicity was made by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay for commercially available hits syringaresinol and cleomiscosin A against lung cancer (A549) cells. The results demonstrated that syringaresinol has an IC50 value of 36.9 μg/mL, while cleomiscosin A has an IC50 value of 133 μg/mL. After MTT, flow cytometry analysis confirmed that compounds induced apoptosis in A549 cells in a dose-dependent manner. This study suggested that the respective lignan compounds can serve as lead candidates for lung cancer therapy via 6-PGD inhibition. Furthermore, in vivo experiments need to be conducted to confirm their efficacy.

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Dracorhodin perchlorate induces apoptosis in bladder cancer cells through Bcl-2, Bcl-XL, survivin down-regulation and caspase-3 activation

Cited by 2 publications

References 29 publications

Effect the Mechanism of Emodin Combined with Cp-1 on Proliferation and Apoptosis of Bladder Cancer Cell Line BIU-87

Effect the Mechanism of Emodin Combined with Cp-1 on Proliferation and Apoptosis of Bladder Cancer Cell Line BIU-87

Identification of Lignan Compounds as New 6-Phosphogluconate Dehydrogenase Inhibitors for Lung Cancer

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