ArticleThe Journal of general virology2016
Newcastle disease virus degrades HIF-1α through proteasomal pathways independent of VHL and p53.
Article in The Journal of general virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Engineering the tumor microenvironment: oncolytic NDV to facilitate CAR-T cell therapy.Journal of translational medicine · 2025Review
- The Potential of Oncolytic Virotherapy in the Treatment of Head and Neck Cancer: A Comprehensive Review.International journal of molecular sciences · 2024Review
- The Viral Knock: Ameliorating Cancer Treatment with Oncolytic Newcastle Disease Virus.Life (Basel, Switzerland) · 2023Review
- KCNJ2/HIF1α positive-feedback loop promotes the metastasis of osteosarcoma.Cell communication and signaling : CCS · 2023Article
- Combining of Oncolytic Virotherapy and Other Immunotherapeutic Approaches in Cancer: A Powerful Functionalization Tactic.Global challenges (Hoboken, NJ) · 2023Review
- Oncolytic Virotherapy in Peritoneal Metastasis Gastric Cancer: The Challenges and Achievements.Frontiers in molecular biosciences · 2022Review
- Impact of Hypoxia over Human Viral Infections and Key Cellular Processes.International journal of molecular sciences · 2021Review
- Review
- Article
- Article
- Systemically Administered Reovirus-Induced Downregulation of Hypoxia Inducible Factor-1α in Subcutaneous Tumors.Molecular therapy oncolytics · 2019Article
- Curcumin suppresses gastric tumor cell growth via ROS-mediated DNA polymerase γ depletion disrupting cellular bioenergetics.Journal of experimental & clinical cancer research : CR · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Newcastle disease virus (NDV) is a candidate agent for oncolytic virotherapy. Despite its potential, the exact mechanism of its oncolysis is still not known. Recently, we reported that NDV exhibited an increased oncolytic activity in hypoxic cancer cells. These types of cells negatively affect therapeutic outcome by overexpressing pro-survival genes under the control of the hypoxia-inducible factor (HIF). HIF-1 is a heterodimeric transcriptional factor consisting of a regulated α (HIF-1α) and a constitutive β subunit (HIF-1β). To investigate the effects of NDV infection on HIF-1α in cancer cells, the osteosarcoma (Saos-2), breast carcinoma (MCF-7), colon carcinoma (HCT116) and fibrosarcoma (HT1080) cell lines were used in the present study. Data obtained showed that a velogenic NDV infection diminished hypoxia-induced HIF-1α accumulation, leading to a decreased activation of its downstream target gene, carbonic anhydrase 9. This NDV-induced downregulation of HIF-1α occurred post-translationally and was partially abrogated by proteasomal inhibition. The process appeared to be independent of the tumour suppressor protein p53. These data revealed a correlation between NDV infection and HIF-1α downregulation, which highlights NDV as a promising agent to eliminate hypoxic cancer cells.
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