ArticleActa neuropathologica communications2019
Downregulation of miR-204 expression defines a highly aggressive subset of Group 3/Group 4 medulloblastomas.
Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Rab24 protein levels show dynamic changes in mouse tissues and human cancers.Cell and tissue research · 2026Article
- The pivotal role of autophagy in the pathogenesis and therapy of medulloblastoma.Future oncology (London, England) · 2024Review
- REST-dependent downregulation of von Hippel-Lindau tumor suppressor promotes autophagy in SHH-medulloblastoma.Scientific reports · 2024Article
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- miRNA-211 maintains metabolic homeostasis in medulloblastoma through its target gene long-chain acyl-CoA synthetase 4.Acta neuropathologica communications · 2023Article
- Review
- Clinical, Histological, and Molecular Prognostic Factors in Childhood Medulloblastoma: Where Do We Stand?Diagnostics (Basel, Switzerland) · 2023Review
- Review
- Integrated Analysis of Transcriptome Data Revealed AURKA and KIF20A as Critical Genes in Medulloblastoma Progression.Frontiers in oncology · 2022Article
- Role of MicroRNAs in the Development and Progression of the Four Medulloblastoma Subgroups.Cancers · 2021Review
- Article
- Recent Advances in Understanding the Role of Autophagy in Paediatric Brain Tumours.Diagnostics (Basel, Switzerland) · 2021Review
- The Role of Noncoding RNAs in the Regulation of Anoikis and Anchorage-Independent Growth in Cancer.International journal of molecular sciences · 2021Review
- Autophagy inhibition impairs the invasion potential of medulloblastoma cells.Molecular biology reports · 2020Article
- Restoration of miR-193a expression is tumor-suppressive in MYC amplified Group 3 medulloblastoma.Acta neuropathologica communications · 2020Article
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide expression profiling studies have identified four core molecular subgroups of medulloblastoma: WNT, SHH, Group 3 and Group 4. Molecular markers are necessary for accurate risk stratification in the non-WNT subgroups due to the underlying heterogeneity in genetic alterations and overall survival. MiR-204 expression was evaluated in molecularly classified 260 medulloblastomas from an Indian cohort and in 763 medulloblastomas from the MAGIC cohort, SickKids, Canada. Low expression of miR-204 in the Group 3 / Group 4 tumors identify a highly aggressive subset of tumors having poor overall survival, in the two independent cohorts of medulloblastomas. Downregulation of miR-204 expression correlates with poor survival within the Group 4 as well indicating it as a valuable risk-stratification marker in the subgroup. Restoration of miR-204 expression in multiple medulloblastoma cell lines was found to inhibit their anchorage-independent growth, invasion potential and tumorigenicity. IGF2R was identified as a novel target of miR-204. MiR-204 expression resulted in downregulation of both M6PR and IGF2R that transport lysosomal proteases from the Golgi apparatus to the lysosomes. Consistent with this finding, miR-204 expression resulted in reduction in the levels of the lysosomal proteases in medulloblastoma cells. MiR-204 expression also resulted in inhibition of autophagy that is known to be dependent on the lysosomal degradation pathway and LC3B, a known miR-204 target. Treatment with HDAC inhibitors resulted in upregulation of miR-204 expression in medulloblastoma cells, suggesting therapeutic role for these inhibitors in the treatment of medulloblastomas. In summary, miR-204 is not only a valuable risk stratification marker in the combined cohort of Group 3 / Group 4 medulloblastomas as well as in the Group 4 itself, that has paucity of good prognostication markers, but also has therapeutic potential as indicated by its tumor suppressive effect on medulloblastoma cells.
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