Neutralization of terminal differentiation in gliomagenesis
Open accessAbstract
An immature state of cellular differentiation—characterized by stem cell–like tendencies and impaired differentiation—is a hallmark of cancer. Using glioblastoma multiforme (GBM) as a model system, we sought to determine whether molecular determinants that drive cells toward terminal differentiation are also genetically targeted in carcinogenesis and whether neutralizing such genes also plays an active role to reinforce the impaired differentiation state and promote malignancy. To that end, we screened 71 genes with known roles in promoting nervous system development that also sustain copy number loss in GBM through antineoplastic assay and identified A2BP1 (ataxin 2 binding protein 1, Rbfox1), an RNA-binding and splicing regulator that is deleted in 10% of GBM cases. Integrated in silico analysis of GBM profiles to elucidate the A2BP1 pathway and its role in glioma identified myelin transcription factor 1-like (Myt1L) as a direct transcriptional regulator of A2BP1. Reintroduction of A2BP1 or Myt1L in GBM cell lines and glioma stem cells profoundly inhibited tumorigenesis in multiple assays, and conversely, shRNA-mediated knockdown of A2BP1 or Myt1L in premalignant neural stem cells compromised neuronal lineage differentiation and promoted orthotopic tumor formation. On the mechanistic level, with the top-represented downstream target TPM1 as an illustrative example, we demonstrated that, among its multiple functions, A2BP1 serves to regulate TPM1’s alternative splicing to promote cytoskeletal organization and terminal differentiation and suppress malignancy. Thus, in addition to the activation of self-renewal pathways, the neutralization of genetic programs that drive cells toward terminal differentiation may also promote immature and highly plastic developmental states that contribute to the aggressive malignant properties of GBM.
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MYT1L loss of function is associated with mental disorders and brain cancer.
“its loss of function is associated with mental disorders and brain cancer13,14.”
From Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis (2025) · cites this paper as [13]
The Results (page not available in our copy) report MYT1L deletion or reduced expression in glioblastoma samples and show that MYT1L knockdown induced tumors in a mouse model, supporting the brain-cancer part. The passage linking genomic alterations to neurodevelopmental and neuropsychiatric disorders concerns A2BP1, not MYT1L; our copy does not establish the claimed MYT1L–mental-disorder association. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMYT1L is expressed lifelong.
“MYT1L is expressed lifelong”
From Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis (2025) · cites this paper as [13]
The Results report MYT1L expression in glioblastoma samples and examine its function in neural stem cells, but do not describe expression across the lifespan. Searches for lifelong expression and expression throughout development and adulthood found no passage establishing the claim. Page numbers were not available in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
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- Authors
- Hu, J., Ho, A. L., Yuan, L., Hu, B., Hua, S., Hwang, S. S., Zhang, J., Hu, T., Zheng, H., Gan, B., Wu, G., Wang, Y. A., Chin, L., & DePinho, R. A.
- Affiliations
- Genomics Medicine (Ireland) (IE)
- Harvard University (US)
- The University of Texas MD Anderson Cancer Center (US)
- Duke University (US)
- Cold Spring Harbor Laboratory (US)
- Experimental Radiation Oncology and
- Joslin Diabetes Center (US)
- Departments of aCancer Biology,
- Genomic Medicine, and
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2013-08-05
- Volume
- 110
- Issue
- 36
- Pages
- 14520-14527
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3767545
- OpenAlex
- W2154312278
- Cited by
- 76
- References
- 52
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 8 · 2021: 5 · 2020: 6 · 2019: 5 · 2018: 6 · 2017: 8 · 2016: 9 · 2015: 5 · 2014: 5 · 2013: 4
- FWCI
- 3.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Funders
- U.S. Department of Defense (K99/R00)
- Leukemia and Lymphoma Society
- Fondation pour la Recherche Médicale
- National Institutes of Health (1k99ca172700-01, K99-R00)
- National Cancer Institute (U01 5U01CA084313, 5K99CA172700, P01 5P01CA095616, U01CA084313, K99 CA172700, P01CA095616)
- DOD Prostate Cancer Research Program
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- glioblastoma, gliomagenesis, terminal differentiation, A2BP1, RBFOX1, MYT1L, TPM1, alternative splicing, RNA-binding proteins, glioma stem cells, neural stem cells, copy number loss, transcriptional regulation, cytoskeletal organization, carcinogenesis
- MeSH terms
- RNA Splicing Factors, Animals, Brain Neoplasms, Cell Differentiation, Cells, Cultured, Female, Glial Fibrillary Acidic Protein, Glioblastoma, Humans, Immunohistochemistry, Mice, Inbred C57BL, Mice, Nude, Mice, Transgenic, Nerve Tissue Proteins, Transcription Factors, Transplantation, Heterologous, Neoplastic Stem Cells, Mice, SCID, RNA-Binding Proteins, Mice, Knockout, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, RNA Interference, Mice, Neural Stem Cells, Carcinogenesis
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