ArticleOncogene2017
MINA controls proliferation and tumorigenesis of glioblastoma by epigenetically regulating cyclins and CDKs via H3K9me3 demethylation.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Protective effect of exercise on metabolic dysfunction‑associated fatty liver disease: Potential epigenetic mechanisms (Review).International journal of molecular medicine · 2025Review
- NKD1 enhances colon cancer progression by inhibiting the autophagic degradation of MYC.Cell death & disease · 2025Article
- Identification of FLYWCH1 as a regulator of platinum-resistance in epithelial ovarian cancer.NAR cancer · 2025Article
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- MDIG-mediated H3K9me3 demethylation upregulates Myc by activating OTX2 and facilitates liver regeneration.Signal transduction and targeted therapy · 2023Article
- The role of histone H3 lysine demethylases in glioblastoma.Cancer metastasis reviews · 2023Review
- MESP2 binds competitively to TCF4 to suppress gastric cancer progression by regulating the SKP2/p27 axis.Cell death discovery · 2023Article
- JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022Review
- First-in-Class Inhibitors of the Ribosomal Oxygenase MINA53.Journal of medicinal chemistry · 2021Article
- Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.Seminars in cancer biology · 2021Review
- Epigenetically Mediated Ciliogenesis and Cell Cycle Regulation, and Their Translational Potential.Cells · 2021Review
- Differential RNA splicing as a potentially important driver mechanism in multiple myeloma.Haematologica · 2021Article
- CSN6 promotes melanoma proliferation and metastasis by controlling the UBR5-mediated ubiquitination and degradation of CDK9.Cell death & disease · 2021Article
- 2-Oxoglutarate-dependent dioxygenases in cancer.Nature reviews. Cancer · 2020Review
- CDGSH Iron Sulfur Domain 2 Deficiency Inhibits Cell Proliferation and Induces Cell Differentiation of Neuroblastoma.Pathology oncology research : POR · 2020Article
- Molecular Signatures ofCancers · 2020Article
- Mdig promotes oncogenic gene expression through antagonizing repressive histone methylation markers.Theranostics · 2020Article
- A CRISPR/Cas9 screen identifies the histone demethylase MINA53 as a novel HIV-1 latency-promoting gene (LPG).Nucleic acids research · 2019Article
- New discoveries of mdig in the epigenetic regulation of cancers.Seminars in cancer biology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is generally known that histone demethylases regulate gene transcription by altering the methylate status on histones, but their roles in cancers and the underlying molecular mechanisms still remain unclear. MYC-induced nuclear antigen (MINA) is reported to be a histone demethylase and highly expressed in many cancers. Here, for the first time, we show that MINA is involved in glioblastoma carcinogenesis and reveal the probable mechanisms of it in cell-cycle control. Kaplan-Meier analysis of progression-free survival showed that high MINA expression was strongly correlated with poor outcome and advancing tumor stage. MINA knockdown significantly repressed the cell proliferation and tumorigenesis abilities of glioblastoma cells in vitro and in vivo that were rescued by overexpressing the full-length MINA afterwards. Microarray analysis after knockdown of MINA revealed that MINA probably regulated glioblastoma carcinogenesis through the predominant cell-cycle pathways. Further investigation showed that MINA deficiency led to a cell-cycle arrest in G1 and G2 phases. And among the downstream genes, we found that cyclins and cyclin-dependent kinases were directly activated by MINA via the demethylation of H3K9me3.
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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.