Pseudolaric Acid B Induced Cell Cycle Arrest, Autophagy and Senescence in Murine Fibrosarcoma L929 Cell

Liu, Chun Yu; Zheng, Gui bin; Zhang, Li Ying; Yan, Ming; Zhang, Wen Yan; Meng, Xian; Yu, Xiao Fang

doi:10.7150/ijms.5726

Cited by 25 publications

(13 citation statements)

References 34 publications

(42 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…But there was no effective drug for therapy and prognosis after surgery. Therefore development of a new and low price drug, especially from traditional Chinese medicine, seems important and urgent, as also previously suggested 26-28. In this study, we found that dracorhodin perchlorate (DP) dose and time-dependently inhibited MCF-7 cell growth, indicating that DP exerted cytotoxic effect on human breast cancer MCF-7 cell.…”

Section: Discussionsupporting

confidence: 58%

Dracorhodin Perchlorate Induced Human Breast Cancer MCF-7 Apoptosis through Mitochondrial Pathways

Yu¹,

Zheng²,

Liu³

et al. 2013

Int. J. Med. Sci.

View full text Add to dashboard Cite

Objective: Dracorhodin perchlorate (DP) was a synthetic analogue of the antimicrobial anthocyanin red pigment dracorhodin. It was reported that DP could induce apoptosis in human prostate cancer, human gastric tumor cells and human melanoma, but the cytotoxic effect of DP on human breast cancer was not investigated. This study would investigate whether DP was a candidate chemical of anti-human breast cancer.Methods: The MTT assay reflected the number of viable cells through measuring the activity of cellular enzymes. Phase contrast microscopy visualized cell morphology. Fluorescence microscopy detected nuclear fragmentation after Hoechst 33258 staining. Flowcytometric analysis of Annexin V-PI staining and Rodamine 123 staining was used to detect cell apoptosis and mitochondrial membrane potential (MMP). Real time PCR detected mRNA level. Western blot examined protein expression.Results: DP dose and time-dependently inhibited the growth of MCF-7 cells. DP inhibited MCF-7 cell growth through apoptosis. DP regulated the expression of Bcl-2 and Bax, which were mitochondrial pathway proteins, to decrease MMP, and DP promoted the transcription of Bax and inhibited Bcl-2. Apoptosis-inducing factor (AIF) and cytochrome c which localized in mitochondrial in physiological condition were released into cytoplasm when MMP was decreased. DP activated caspase-9, which was the downstream of mitochondrial pathway. Therefore DP decreased MMP to release AIF and cytochrome c into cytoplasm, further activating caspase 9, lastly led to apoptosis.Conclusion: Therefore DP was a candidate for anti-breast cancer, DP induced apoptosis of MCF-7 through mitochondrial pathway.

show abstract

Section: Discussionsupporting

confidence: 58%

Dracorhodin Perchlorate Induced Human Breast Cancer MCF-7 Apoptosis through Mitochondrial Pathways

Yu¹,

Zheng²,

Liu³

et al. 2013

Int. J. Med. Sci.

View full text Add to dashboard Cite

show abstract

“…To confirm that G2/M synchronization inhibits EV-D68 and EV-A71, we assessed the effects of an alternate agent that can exert G2/M arrest in vitro , pseudolaric acid B (PAB), which is a diterpene acid isolated from the root and trunk bark of Pseudolarix kaempferi Grord (Pinaceae) (Yu et al, 2007 , 2013 ). PAB was confirmed to promote G2/M arrest after 24 h (Figure 6C ).…”

Section: Resultsmentioning

confidence: 99%

“…To further analyze the mechanism of host cell cycle manipulation by EV-D68, we assessed the expression of cyclins and CDKs that are known to form complexes to regulate cell cycle progression (Oosthuysen et al, 2015 ). For example: cyclinD/CDK4 and cyclinD/CDK6 regulate G0/G1 progression (Massagué, 2004 ); cyclinE/CDK2 regulates S-phase entry from G1 (Hinds et al, 1992 ); cyclinA/CDK2 regulates S-phase progression by replacing cyclinE (Coverley et al, 2002 ; Yam et al, 2002 ); and cyclinB1/CDK1 prevents cell cycle transition from G2/M into G0/G1 (Yu et al, 2013 ; Adeyemi and Pintel, 2014 ). We demonstrated that cyclinD, CDK4, CDK6, cyclinE1 and CDK2 are down-regulated after EV-D68 infection, which could explain the ability of EV-D68 to inhibit the transition from G0/G1 to S phase.…”

Section: Discussionmentioning

confidence: 99%

Human Enterovirus 68 Interferes with the Host Cell Cycle to Facilitate Viral Production

Wang

Zhong

Wang

et al. 2017

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Enterovirus D68 (EV-D68) is an emerging pathogen that recently caused a large outbreak of severe respiratory disease in the United States and other countries. Little is known about the relationship between EV-D68 virus and host cells. In this study, we assessed the effect of the host cell cycle on EV-D68 viral production, as well as the ability of EV-D68 to manipulate host cell cycle progression. The results suggest that synchronization in G0/G1 phase, but not S phase, promotes viral production, while synchronization in G2/M inhibits viral production. Both an early EV-D68 isolate and currently circulating strains of EV-D68 can manipulate the host cell cycle to arrest cells in the G0/G1 phase, thus providing favorable conditions for virus production. Cell cycle regulation by EV-D68 was associated with corresponding effects on the expression of cyclins and CDKs, which were observed at the level of the protein and/or mRNA. Furthermore, the viral non-structural protein 3D of EV-D68 prevents progression from G0/G1 to S. Interestingly, another member of the Picornaviridae family, EV-A71, differs from EV-D68 in that G0/G1 synchronization inhibits, rather than promotes, EV-A71 viral replication. However, these viruses are similar in that G2/M synchronization inhibits the production and activity of both viruses, which is suggestive of a common therapeutic target for both types of enterovirus. These results further clarify the pathogenic mechanisms of enteroviruses and provide a potential strategy for the treatment and prevention of EV-D68-related disease.

show abstract

“…The samples were analysed by BD FACSVerse (BD Biosciences) using BD FACSuite software. At least 20,000 events were analysed and recorded [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

Para-Phenylenediamine Induces Apoptotic Death of Melanoma Cells and Reduces Melanoma Tumour Growth in Mice

Bhowmick

Bhar

Mallick³

et al. 2016

Biochemistry Research International

View full text Add to dashboard Cite

Melanoma is one of the most aggressive forms of cancer, usually resistant to standard chemotherapeutics. Despite a huge number of clinical trials, any success to find a chemotherapeutic agent that can effectively destroy melanoma is yet to be achieved. Para-phenylenediamine (p-PD) in the hair dyes is reported to purely serve as an external dyeing agent. Very little is known about whether p-PD has any effect on the melanin producing cells. We have demonstrated p-PD mediated apoptotic death of both human and mouse melanoma cells in vitro. Mouse melanoma tumour growth was also arrested by the apoptotic activity of intraperitoneal administration of p-PD with almost no side effects. This apoptosis is shown to occur primarily via loss of mitochondrial membrane potential (MMP), generation of reactive oxygen species (ROS), and caspase 8 activation. p-PD mediated apoptosis was also confirmed by the increase in sub-G0/G1 cell number. Thus, our experimental observation suggests that p-PD can be a potential less expensive candidate to be developed as a chemotherapeutic agent for melanoma.

show abstract

Pseudolaric Acid B Induced Cell Cycle Arrest, Autophagy and Senescence in Murine Fibrosarcoma L929 Cell

Cited by 25 publications

References 34 publications

Dracorhodin Perchlorate Induced Human Breast Cancer MCF-7 Apoptosis through Mitochondrial Pathways

Dracorhodin Perchlorate Induced Human Breast Cancer MCF-7 Apoptosis through Mitochondrial Pathways

Human Enterovirus 68 Interferes with the Host Cell Cycle to Facilitate Viral Production

Para-Phenylenediamine Induces Apoptotic Death of Melanoma Cells and Reduces Melanoma Tumour Growth in Mice

Contact Info

Product

Resources

About