Bcl-2 Overexpression Inhibits Generation of Intracellular Reactive Oxygen Species and Blocks Adriamycin-induced Apoptosis in Bladder Cancer Cells

Kong, Chuize; Zhang, Zhe

doi:10.7314/apjcp.2013.14.2.895

Cited by 19 publications

(13 citation statements)

References 30 publications

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“…Leukemia types in which Bcl-2 is overexpressed have a poor prognosis and they have traditionally been related to chemoresistance, emphasizing the importance of this finding [ 7 , 39 ]. Indeed, Bcl-2 overexpression in leukemia types confers resistance to a wide range of antineoplastic drugs [ 40 – 44 ] and this phenomenon has also been observed in other cancers [ 11 ]. Metformin has very low toxicity and it does not affect the growth, differentiation, or survival of normal hematopoietic precursors, even at the concentrations up to 120 mM [ 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

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Metformin Induces Cell Cycle Arrest and Apoptosis in Drug-Resistant Leukemia Cells

Rodríguez-Lirio

Pérez‐Yarza

Fernández-Suárez

et al. 2015

Leukemia Research and Treatment

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Recent epidemiological studies indicate that the antidiabetic drug metformin has chemosensitizing and chemopreventive effects against carcinogenesis. Here, we demonstrate that metformin exerts varying degrees of antitumor activity against human leukemia cells, as reflected by differences in growth inhibition, apoptosis, and alterations to metabolic enzymes. In metformin-sensitive cells, autophagy was not induced but rather it blocked proliferation by means of arresting cells in the S and G2/M phases which was associated with the downregulation of cyclin A, cyclin B1, and cdc2, but not that of cyclin E. In 10E1-CEM cells that overexpress Bcl-2 and are drug-resistant, the effect of metformin on proliferation was more pronounced, also inducing the activation of the caspases 3/7 and hence apoptosis. In all sensitive cells, metformin decreased the Δψ m and it modified the expression of enzymes involved in energy metabolism: PKCε (PKCepsilon) and PKCδ (PKCdelta). In sensitive cells, metformin altered PKCε and PKCδ expression leading to a predominance of PKCε over PKCδ which implies a more glycolytic state. The opposite occurs in the nonresponsive cells. In conclusion, we provide new insights into the activity of metformin as an antitumoral agent in leukemia cells that could be related to its capability to modulate energy metabolism.

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Section: Discussionmentioning

confidence: 99%

“…The resistant phenotype represents an adaptive response of cancer cells and it is characterized by alterations to multiple pathways, among which metabolic alterations might play an important role [ 6 ]. In T-ALL, Bcl-2 overexpression or mutations in the PTEN protein are related to resistance [ 7 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

Metformin Induces Cell Cycle Arrest and Apoptosis in Drug-Resistant Leukemia Cells

Rodríguez-Lirio

Pérez‐Yarza

Fernández-Suárez

et al. 2015

Leukemia Research and Treatment

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“…Cerebral ischemia reperfusion injury is conventional case in clinical, the event can cause a large number of neuronal apoptosis, greater harm to the patients [12]. Establishing cerebral ischemia-reperfusion model, in order to simulate the human ischemia-reperfusion injury, to identify the agents can greatly reduce the cerebral ischemia injury, to reduce the suffering of patients and to improve their quality of life [13]. In this study, the suture method which establish cerebral ischemia, clinical model of infarction very similar to humans, has high research value [14].…”

Section: Discussionmentioning

confidence: 99%

Effect of Rabdosia Rubescens Total Flavonoids on Cerebral Ischemic Reperfusion Model Mice

Li¹,

Shao²,

Miao³

2018

dtbh

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Abstract. Objective: To study the protective effects of Rabdosia rubescens total flavonoids (RRTF) on the cerebral ischemia reperfusion model(CIRM) of mice. Methods: By blocking bilateral carotid artery blood flow, the mice model of CIRM were established. Before surgery, medicines were given once a day for 7 successive days. The model was constructed after one hour of the last administration, 24h reperfusion after surgery. Measuring LD, LDH and ATP enzyme of mouse brain tissue, and observing morphological changes of brain tissue. Results: Each dose group of RRTF can significantly lower mortality, reduce the content of LD, ease brain tissue damage while can obviously improve the vitality of LDH, enhance the enzyme activity in mice with cerebral ischemia reperfusion injury, such as Na + -K + -ATPase, Mg 2+ -ATPase, Ca 2+ -ATPase. Conclusions: Indicators among each dose of the Rabdosia rubescens flavonoids on cerebral ischemia reperfusion model have better improvement, large doses is the best.

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“…The BAX gene expression appoints the cells' life or death decision, which is affected by ROS values. On the other hand, an anti‐apoptotic gene called BCL2 makes the cell capable of bypass apoptotic death under different destructive stresses . M. Song et al demonstrated the significant BCL2 down‐regulation in the presence of vitamin C (strong antioxidant agent).…”

Section: Introductionmentioning

confidence: 99%

Green‐synthesized Zinc oxide nanoparticle, an efficient safe anticancer compound for human breast MCF7 cancer cells

Salari

Neamati

Tabrizi

et al. 2019

Applied Organom Chemis

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There are many types of researches investigating anticancer therapeutics for breast cancer therapy. Zinc oxide nanoparticles (ZnONPs) as an efficient drug delivery system, has been widely being used in various biomedical applications. In the current study, we synthesized ZnONP applying Rheum rhaponticum Waste (RRW) as a novel bio‐platform to investigate its anticancer impacts on MCF7 breast cancer cells compared with normal Human HFF and HDF cells. In this regard, RRW was triggered to synthesize the ZnONPs. Then, they were characterized by XRD, FTIR, TEM, and SEM analysis. Next, the MCF‐7, HFF, and HDF cell lines were cultured and treated as the following plane: Incubation of all cell lines for 72, 48, and 24 hours at the presence of different ZnONPs doses. Finally, the cell morphology, BCL2‐ BAX genes expression profile and AO/PI‐fluorescent cell staining on the 48‐hour incubated cells were analyzed to check the ZnONP apoptotic activity. Moreover, the ZnONP antioxidant activity was analyzed by a DPPH antioxidant test. We produced the 30 nm ZnONPs which significantly increased the BAX and decreased the BCL‐2 gene expression. According to the results including the Sub G1 enhancement peaks, apoptotic hallmarks, MTT assay, and the AO/PI‐fluorescent stained cells, ZnONPs can specifically induce apoptotic death in MCF7 breast cancer cells compared with normal HFF and HDF cells. The IC50 values of MCF‐7 in 72, 48, and 24 hr were measured at 8, 11, and 12 μg/ml in 72, 48, and 24 hr, respectively. This is while the mentioned values in the normal cells (HFF, HDF) were estimated at higher treatment doses. In conclusion, we suggest that the ZnONPs have the potential to be applied as a safe cell‐specific apoptosis inducer in breast cancer treatment. However, there are many challenges that need to be clarified for applying them as an efficient anticancer agent.

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Bcl-2 Overexpression Inhibits Generation of Intracellular Reactive Oxygen Species and Blocks Adriamycin-induced Apoptosis in Bladder Cancer Cells

Abstract: Resistance to induction of apoptosis is a major obstacle for bladder cancer treatment. Bcl-2 is thought to be involved in anti-apoptotic signaling. In this study, we investigated the effect of Bcl-2 overexpression on apoptotic resistance and intracellular reactive oxygen species (

Cited by 19 publications

References 30 publications

Metformin Induces Cell Cycle Arrest and Apoptosis in Drug-Resistant Leukemia Cells

Metformin Induces Cell Cycle Arrest and Apoptosis in Drug-Resistant Leukemia Cells

Effect of Rabdosia Rubescens Total Flavonoids on Cerebral Ischemic Reperfusion Model Mice

Green‐synthesized Zinc oxide nanoparticle, an efficient safe anticancer compound for human breast MCF7 cancer cells

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