ArticleHuman gene therapy2014
Epithelial-mesenchymal transition enhances response to oncolytic herpesviral therapy through nectin-1.
Article in Human gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Oncolytic adenovirus in treating malignant ascites: A phase II trial and longitudinal single-cell study.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Trial
- Oncolytic viruses: A novel therapeutic approach for pancreatic cancer.Molecular therapy. Oncology · 2025Review
- Functional and in silico evidence for the role of microRNAs 148a-5p and 199a in migration and invasion of papillary thyroid carcinoma cells.Discover oncology · 2025Article
- Minute virus of mice shows oncolytic activity against pancreatic cancer cells exhibiting a mesenchymal phenotype.Molecular therapy. Oncology · 2024Article
- Virus-inspired strategies for cancer therapy.Seminars in cancer biology · 2022Review
- Knowledge-graph-based cell-cell communication inference for spatially resolved transcriptomic data with SpaTalk.Nature communications · 2022Article
- Role of immunotherapy in Ewing sarcoma.Journal for immunotherapy of cancer · 2020Review
- Tumor-Associated Macrophage Status in Cancer Treatment.Cancers · 2020Review
- Myelolytic Treatments Enhance Oncolytic Herpes Virotherapy in Models of Ewing Sarcoma by Modulating the Immune Microenvironment.Molecular therapy oncolytics · 2018Article
- Oncolytic Virotherapy versus Cancer Stem Cells: A Review of Approaches and Mechanisms.Cancers · 2018Review
- Corneal Epithelial Cells Exhibit Myeloid Characteristics and Present Antigen via MHC Class II.Investigative ophthalmology & visual science · 2018Article
- Identification of SSEA-1 expressing enhanced reprogramming (SEER) cells in porcine embryonic fibroblasts.Cell cycle (Georgetown, Tex.) · 2017Article
- Tumor-Associated Macrophages in Oncolytic Virotherapy: Friend or Foe?Biomedicines · 2016Review
- Assessment of oncolytic HSV efficacy following increased entry-receptor expression in malignant peripheral nerve sheath tumor cell lines.Gene therapy · 2014Article
- Targeting the hallmarks of cancer with therapy-induced endoplasmic reticulum (ER) stress.Molecular & cellular oncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cancers exhibiting epithelial-mesenchymal transition (EMT) are associated with aggressive behavior and increased metastatic potential. Therapies that are able to target EMT would have significant clinical value. Nectin-1 is a cell surface herpes simplex virus type 1 (HSV-1) receptor that also forms a component of intercellular adherens junctions, which are typically disrupted in EMT. To explore relationships between HSV-1 sensitivity and EMT, we generated cell lines with a stable EMT phenotype from human follicular thyroid cancer (WRO82-1) through E-cadherin silencing with short hairpin RNA (shEcadWRO). HSV-1 viral attachment and gene expression were both enhanced in shEcadWRO as compared with shControl. Immunoblotting and immunostaining revealed enhanced nectin-1 expression by shEcadWRO. Receptor-blocking assays demonstrated that increased herpesviral entry into shEcadWRO as compared with shControl was mediated predominantly through nectin-1. Colocalization of green fluorescent protein-tagged HSV-1 and tdTomato-tagged nectin-1 confirmed an increase in viral attachment to nectin-1 in shEcadWRO. Cell viability assays demonstrated increased susceptibility of shEcadWRO to HSV-1 oncolysis, and a murine flank tumor model showed significantly enhanced regression of shEcadWRO tumors in response to oncolytic HSV-1 as compared with control tumors. A separate model of EMT induction through transforming growth factor-β stimulation confirmed enhanced HSV-1 susceptibility in Panc1 cells. These results demonstrate that the process of EMT leads to increased herpesviral susceptibility through enhanced cell surface nectin-1 expression, suggesting that cancers exhibiting EMT may be naturally sensitive targets for herpesviral therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.