Newcastle disease virus suppress glycolysis pathway and induce breast cancer cells death.
Cancer metabolism
Oncolytics
Pyruvate
Virotherapy
Warburg effect
Journal
Virusdisease
ISSN: 2347-3584
Titre abrégé: Virusdisease
Pays: India
ID NLM: 101624144
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
17
01
2020
accepted:
18
06
2020
entrez:
9
9
2020
pubmed:
10
9
2020
medline:
10
9
2020
Statut:
ppublish
Résumé
Newcastle disease virus (NDV) can modulate cancer cell signaling pathway and induce apoptosis in cancer cells. Cancer cells increase their glycolysis rates to meet the energy demands for their survival and generate ATP as the primary energy source for cell growth and proliferation. Interfering the glycolysis pathway may be a valuable antitumor strategy. This study aimed to assess the effect of NDV on the glycolysis pathway in infected breast cancer cells. Oncolytic NDV attenuated AMHA1 strain was used in this study. AMJ13 and MCF7 breast cancer cell lines and a normal embryonic REF cell line were infected with NDV with different multiplicity of infections (moi) to determine the IC50 of NDV through MTT assay. Crystal violet staining was done to study the morphological changes. NDV apoptosis induction was assessed using AO/PI assay. NDV interference with the glycolysis pathway was examined through measuring hexokinase (HK) activity, pyruvate, and ATP concentrations, and pH levels in NDV infected and non-infected breast cancer cells and in normal embryonic cells. The results showed that NDV replicates efficiently in cancer cells and spare normal cells and induce morphological changes and apoptosis in breast cancer cells but not in normal cells. NDV infected cancer cells showed decreased in the HK activity, pyruvate and ATP concentrations, and acidity, which reflect a significant decrease in the glycolysis activity of the NDV infected tumor cells. No effects on the normal cells were observed. In conclusion, oncolytic NDV ability to reduce glycolysis pathway activity in cancer cells can be an exciting module to improve antitumor therapeutics.
Identifiants
pubmed: 32904847
doi: 10.1007/s13337-020-00612-z
pii: 612
pmc: PMC7458979
doi:
Types de publication
Journal Article
Langues
eng
Pagination
341-348Informations de copyright
© Indian Virological Society 2020.
Déclaration de conflit d'intérêts
Conflict of interestThe authors disclose no potential conflict of interest.
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