ArticleJournal of neuro-oncology2021
GliPR1 knockdown by RNA interference exerts anti-glioma effects in vitro and in vivo.
Article in Journal of neuro-oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Stochastic Nanoscale Biophysical Cues as a Basis for the Induction of Glioblastoma-Like Transcriptional Programs in Astrocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multi-omics and mendelian randomization uncover microbial-metabolite-gene interactions in age-related hearing loss.AMB Express · 2026Article
- Identification and validation of glucocorticoid receptor and programmed cell death-related genes in spinal cord injury using machine learning.Scientific reports · 2025Article
- Extracellular adenosine oppositely regulates the purinome machinery in glioblastoma and mesenchymal stem cells.IUBMB life · 2024Article
- CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024Review
- Expression and Genetic Effects of GLI Pathogenesis-Related 1 Gene on Backfat Thickness in Pigs.Genes · 2022Article
- Surfaceome Proteomic of Glioblastoma Revealed Potential Targets for Immunotherapy.Frontiers in immunology · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
introductionIn human glioblastomas, glioma pathogenesis-related protein1 (GliPR1) is overexpressed and appears to be an oncoprotein. We investigated whether GliPR1 knockdown in glioma cells by RNA interference exerts anti-glioma effects.
methodsExperiments used human glioblastoma cell lines transduced with GliPR1 shRNA (sh#301, sh#258). Transduction produced stringent doxycycline-dependent GliPR1 knockdown in clones (via lentiviral "all-in-one" TetOn-shRNA vector) or stable GliPR1 knockdown in polyclonal cells (via constitutive retroviral-shRNA vector). In vitro assessments included cellular proliferation and clonogenic survival. In vivo assessments in tumor-bearing nude mice included tumor growth and survival.
resultsUsing doxycycline-dependent GliPR1 knockdown, shGliPR1-transduced U87-MG clones demonstrated reductions in cellular proliferation in the presence versus absence of doxycycline. Using stable GliPR1 knockdown, polyclonal shGliPR1-transduced U87-MG, A172, and U343-MG cells consistently showed decreased clonogenic survival and induced apoptosis (higher proportion of early apoptotic cells) compared to control shLuc-transduced cells. In tumor-bearing nude mice, using doxycycline-dependent GliPR1 knockdown, subcutaneous and cranial transplantation of the U87-MG clone 980-5 (transduced with GliPR1 sh#301) resulted in reduced subcutaneous tumor volume and cerebral tumor area in doxycycline-treated mice versus those left untreated. Using stable GliPR1 knockdown, nude mice cranially transplanted with polyclonal U87-MG cells transduced with GliPR1 sh#258 had significantly prolonged survival compared to mice cranially transplanted with control shLuc-transduced cells (41 versus 26 days; P < 0.001).
conclusionGliPR1 knockdown in glioma cells decreased cellular proliferation, decreased clonogenic survival, and induced apoptosis in vitro, and reduced glioblastoma tumor growth and prolonged survival in vivo. These findings support that GliPR1 may have potential value as a therapeutic target.
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