ArticleOncotarget2017
Alternative RNA splicing of the MEAF6 gene facilitates neuroendocrine prostate cancer progression.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Identification and In Silico Characterization of an Alternatively Spliced Novel Transcript of Human DDR2 Gene.Cell biochemistry and biophysics · 2026Article
- ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis.Nature communications · 2025Article
- New Insights into Potential Therapeutic Targets for Neuroendocrine Prostate Cancer: From Bench to Clinic.Research (Washington, D.C.) · 2025Review
- Splicing Modulation Results in Aberrant Isoforms and Protein Products of p53 Pathway Genes and the Sensitization of B Cells to Non-Genotoxic MDM2 Inhibition.International journal of molecular sciences · 2023Article
- Aggressive variants of prostate cancer: underlying mechanisms of neuroendocrine transdifferentiation.Journal of experimental & clinical cancer research : CR · 2022Review
- Functional analysis of the 1p34.3 risk locus implicates GNL2 in high-grade serous ovarian cancer.American journal of human genetics · 2022Article
- Molecular events in neuroendocrine prostate cancer development.Nature reviews. Urology · 2021Review
- Review
- MACF1 promotes osteoblast differentiation by sequestering repressors in cytoplasm.Cell death and differentiation · 2021Article
- The evolutionarily conserved long non-coding RNA LINC00261 drives neuroendocrine prostate cancer proliferation and metastasis via distinct nuclear and cytoplasmic mechanisms.Molecular oncology · 2021Article
- Intron retention is a hallmark and spliceosome represents a therapeutic vulnerability in aggressive prostate cancer.Nature communications · 2020Article
- Pathway-guided analysis identifies Myc-dependent alternative pre-mRNA splicing in aggressive prostate cancers.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Review
- The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer.BioMed research international · 2020Article
- Alternative RNA splicing of the GIT1 gene is associated with neuroendocrine prostate cancer.Cancer science · 2019Article
- A novel mechanism of SRRM4 in promoting neuroendocrine prostate cancer development via a pluripotency gene network.EBioMedicine · 2018Article
- Roles of Alternative RNA Splicing of the Bif-1 Gene by SRRM4 During the Development of Treatment-induced Neuroendocrine Prostate Cancer.EBioMedicine · 2018Article
- Prostate cancer susceptibility and growth linked to Y chromosome genes.Frontiers in bioscience (Elite edition) · 2018Review
- Development of Neuroendocrine Prostate Cancers by the Ser/Arg Repetitive Matrix 4-Mediated RNA Splicing Network.Frontiers in oncology · 2018Article
- Establishment of a neuroendocrine prostate cancer model driven by the RNA splicing factor SRRM4.Oncotarget · 2017Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although potent androgen receptor pathway inhibitors (ARPI) improve overall survival of metastatic prostate cancer patients, treatment-induced neuroendocrine prostate cancer (t-NEPC) as a consequence of the selection pressures of ARPI is becoming a more common clinical issue. Improved understanding of the molecular biology of t-NEPC is essential for the development of new effective management approaches for t-NEPC. In this study, we identify a splice variant of the MYST/Esa1-associated factor 6 (MEAF6) gene, MEAF6-1, that is highly expressed in both t-NEPC tumor biopsies and neuroendocrine cell lines of prostate and lung cancers. We show that MEAF6-1 splicing is stimulated by neuronal RNA splicing factor SRRM4. Rather than inducing neuroendocrine trans-differentiation of cells in prostate adenocarcinoma, MEAF6-1 upregulation stimulates cell proliferation, anchorage-independent cell growth, invasion and xenograft tumor growth. Gene microarray identifies that these MEAF6-1 actions are in part mediated by the ID1 and ID3 genes. These findings suggest that the MEAF6-1 variant does not induce neuroendocrine differentiation of prostate cancer cells, but rather facilitates t-NEPC progression by increasing the proliferation rate of cells that have acquired neuroendocrine phenotypes.
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