ArticleBrain pathology (Zurich, Switzerland)2020
MiR-1253 exerts tumor-suppressive effects in medulloblastoma via inhibition of CDK6 and CD276 (B7-H3).
Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- B7-H3 membranous expression correlates with histological grading in a two-center cohort of 133 pre-treatment bone and soft tissue sarcoma samples.BMC cancer · 2026Article
- Targeting Androgen Receptor as a Novel Radiosensitizing Therapy to Improve Long-Term Survival and Anti-tumor Immunity in Glioblastoma via TGF-β/Smad3 Axis Reprogramming.Research square · 2026Article
- Anti-cancer immune priming with β-radioligand therapy using a novel high affinity antibody selectively targeting the 4Ig-Isoform of B7-H3.Theranostics · 2026Article
- Immune checkpoint inhibitors in medulloblastoma: current updates in preclinical and clinical developments.Frontiers in oncology · 2026Review
- Decoding the immune microenvironment: precision immunotherapy for medulloblastoma subtypes.Frontiers in immunology · 2026Review
- Targeting TET3 suppresses group 3 medulloblastoma stemness and progression via impairing hypomethylation of Otx2 super-enhancer.Cell reports. Medicine · 2025Article
- microRNA Expression in the Late Embryonic Pax6-Null Mouse Cerebellum.Molecular neurobiology · 2025Article
- High B7-H3 protein expression in Medulloblastoma is associated with metastasis and unfavorable patient outcomes.Diagnostic pathology · 2025Article
- MiRNAs as major players in brain health and disease: current knowledge and future perspectives.Cell death discovery · 2025Review
- Medulloblastoma: biology and immunotherapy.Frontiers in immunology · 2025Review
- Tumor Immunotherapy Targeting B7-H3: From Mechanisms to Clinical Applications.ImmunoTargets and therapy · 2025Review
- CircSEC24A induces KLF8 expression to promote the malignant progression of non-small cell lung cancer by regulating miR-1253.Thoracic cancer · 2024Article
- Identification of MicroRNA Profiles in Fetal Spina Bifida: The Role in Pathomechanism and Diagnostic Significance.International journal of molecular sciences · 2024Article
- A promising target for breast cancer: B7-H3.BMC cancer · 2024Review
- B7-H3 in glioblastoma and beyond: significance and therapeutic strategies.Frontiers in immunology · 2024Review
- MicroRNA-1 attenuates the growth and metastasis of small cell lung cancer through CXCR4/FOXM1/RRM2 axis.Molecular cancer · 2023Article
- The Features of Immune Checkpoint Gene Regulation by microRNA in Cancer.International journal of molecular sciences · 2022Review
- Identification of PBK as a hub gene and potential therapeutic target for medulloblastoma.Oncology reports · 2022Article
- EIF4A3-induced circFIP1L1 represses miR-1253 and promotes radiosensitivity of nasopharyngeal carcinoma.Cellular and molecular life sciences : CMLS · 2022Article
- Pediatric medulloblastoma express immune checkpoint B7-H3.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
Abstract
Of the four primary subgroups of medulloblastoma, the most frequent cytogenetic abnormality, i17q, distinguishes Groups 3 and 4 which carry the highest mortality; haploinsufficiency of 17p13.3 is a marker for particularly poor prognosis. At the terminal end of this locus lies miR-1253, a brain-enriched microRNA that regulates bone morphogenic proteins during cerebellar development. We hypothesized miR-1253 confers novel tumor-suppressive properties in medulloblastoma. Using two different cohorts of medulloblastoma samples, we first studied the expression and methylation profiles of miR-1253. We then explored the anti-tumorigenic properties of miR-1253, in parallel with a biochemical analysis of apoptosis and proliferation, and isolated oncogenic targets using high-throughput screening. Deregulation of miR-1253 expression was noted, both in medulloblastoma clinical samples and cell lines, by epigenetic silencing via hypermethylation; specific de-methylation of miR-1253 not only resulted in rapid recovery of expression but also a sharp decline in tumor cell proliferation and target gene expression. Expression restoration also led to a reduction in tumor cell virulence, concomitant with activation of apoptotic pathways, cell cycle arrest and reduction of markers of proliferation. We identified two oncogenic targets of miR-1253, CDK6 and CD276, whose silencing replicated the negative trophic effects of miR-1253. These data reveal novel tumor-suppressive properties for miR-1253, i.e., (i) loss of expression via epigenetic silencing; (ii) negative trophic effects on tumor aggressiveness; and (iii) downregulation of oncogenic targets.
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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.