ArticleNeuro-oncology2016
Neurotensin signaling stimulates glioblastoma cell proliferation by upregulating c-Myc and inhibiting miR-29b-1 and miR-129-3p.
Article in Neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
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- CXCR4+ circulating tumor cells (CTCs) accumulate in subcutaneous, immune suppressive, CXCL12-loaded-hydrogel.Materials today. Bio · 2026Article
- KPNA2 promotes lung adenocarcinoma progression by inducing glycolysis-assisted MYC nuclear translocation.Cytotechnology · 2025Article
- Matrine alkaloids modulating DNA damage repair in chemoresistant non-small cell lung cancer cells.BMC cancer · 2024Article
- Glioma and Peptidergic Systems: Oncogenic and Anticancer Peptides.International journal of molecular sciences · 2024Review
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- LIN28B and Let-7 in Diffuse Midline Glioma: A Review.Cancers · 2023Review
- Design, Synthesis, and Biological Evaluation of the First Radio-Metalated Neurotensin Analogue Targeting Neurotensin Receptor 2.ACS omega · 2023Article
- Role of microRNA-494 in tumor progression.American journal of translational research · 2023Review
- Review
- LncRNA MAPKAPK5_AS1 facilitates cell proliferation in hepatitis B virus -related hepatocellular carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer.Biomedicines · 2021Review
- Transcription Factor DLX5 Promotes Hair Follicle Stem Cell Differentiation by Regulating the c-MYC/microRNA-29c-3p/NSD1 Axis.Frontiers in cell and developmental biology · 2021Article
- Profiles of immune cell infiltration and immune-related genes in the tumor microenvironment of HNSCC with or without HPV infection.American journal of translational research · 2021Article
- Lnc-GD2H Promotes Proliferation by Forming a Feedback Loop With c-Myc and Enhances Differentiation Through Interacting With NACA to Upregulate Myog in C2C12 Myoblasts.Frontiers in cell and developmental biology · 2021Article
- Bombesin Receptor Family Activation and CNS/Neural Tumors: Review of Evidence Supporting Possible Role for Novel Targeted Therapy.Frontiers in endocrinology · 2021Review
- The role of Neurotensin and its receptors in non-gastrointestinal cancers: a review.Cell communication and signaling : CCS · 2020Review
- Use of Genome-Scale Integrated Analysis to Identify Key Genes and Potential Molecular Mechanisms in Recurrence of Lower-Grade Brain Glioma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- In silico analysis identified miRNA‑based therapeutic agents against glioblastoma multiforme.Oncology reports · 2019Article
- Sortilin promotes glioblastoma invasion and mesenchymal transition through GSK-3β/β-catenin/twist pathway.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeurotensin (NTS) and its primary receptor NTSR1 are implicated in cancer progression. Aberrant expression of NTS/NTSR1 contributes to the proliferation of glioblastoma cells; however, the mechanism is not fully understood.
methodsMicroarray and real-time PCR were performed to identify the NTS-regulated micro (mi)RNAs. The targets of the miRNAs were identified by luciferase assays and immunoblot analysis. The c-Myc binding sites in the miR-29b-1 and cyclin-dependent kinase (CDK)4 promoters were identified through chromatin immunoprecipitation assay. Cell proliferation was evaluated by Cell Counting Kit-8 assay and flow cytometry analysis. An orthotopic xenograft model demonstrated the role of NTS/NTSR1 and miRNAs in glioblastoma growth in vivo.
resultsPharmacological inhibition or small interfering NTSR1 treatment blocked glioblastoma cell cycle progression in the G1 phase with a concomitantly decreased expression of CDK6, CDK4, and c-Myc. Knockdown of NTSR1 increased the expression of miR-29b-1 and miR-129-3p, which were responsible for the decreased CDK6 expression. NTS/NTSR1 signaling activated the transcription factor c-Myc in U87 cells, leading to increased CDK4 expression and repressed miR-29b-1 expression. Knockdown of NTSR1 decreased the glioblastoma growth in vivo and significantly prolonged the survival time of the tumor-bearing mice, an effect that can be largely reversed by antagomir.
conclusionsOur study showed a novel regulatory mechanism of NTS/NTSR1, an upstream signaling of miRNAs and c-Myc, in glioblastoma progression. The inhibition of the NTSR1 function or the upregulation of miR-29b-1 and miR-129-3p expression impaired glioma cell proliferation. These results suggested that the NTS/NTSR1/c-Myc/miRNA axis may be a potential therapeutic target for glioblastoma therapy.
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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.