ReviewCell cycle (Georgetown, Tex.)2018
Neat-en-ing up our understanding of p53 pathways in tumor suppression.
Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- NEAT1 repression by MED12 creates chemosensitivity in p53 wild-type breast cancer cells.The FEBS journal · 2024Article
- The long non-coding RNA NEAT1 is a ΔNp63 target gene modulating epidermal differentiation.Nature communications · 2023Article
- Context-Dependent Function of Long Noncoding RNAMolecular and cellular biology · 2022Article
- Inadvertent Transfer of Murine VL30 Retrotransposons to CAR-T Cells.Advances in cell and gene therapy · 2022Article
- SOX9-transactived long non-coding RNA NEAT1 promotes the self-renewal of liver cancer stem cells through PKA/Hippo signaling.Signal transduction and targeted therapy · 2021Article
- NEAT1 on the Field of Parkinson's Disease: Offense, Defense, or a Player on the Bench?Journal of Parkinson's disease · 2021Review
- The Long Noncoding RNAMolecular cancer research : MCR · 2020Article
- Long noncoding RNAs: p53's secret weapon in the fight against cancer?PLoS biology · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Although the p53 transcription factor has a well-established role in tumor suppression, little is known about how the non-coding targets of p53 mediate its tumor suppression function. Analysis of ncRNAs regulated by p53 revealed Neat1 as a direct p53 target gene. Neat1 has physiological roles in the development and differentiation of the mammary gland and corpus luteum, but its roles in cancer have been conflicting. To unequivocally understand Neat1 function in cancer, we used Neat1 null mice. Interestingly, we found that Neat1 deficiency promotes transformation both in oncogene-expressing fibroblasts and in a mouse model for pancreatic cancer. Specifically, Neat1 loss in the pancreas results in the enhanced development of preneoplastic lesions associated with dampened expression of differentiation genes. While the exact mechanisms underlying tumor suppression are unknown, there are several described mechanisms that may be responsible for Neat1-mediated tumor suppression. Collectively, these findings suggest that Neat1 enforces differentiation to suppress pancreatic cancer.
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What OpenQuestion holds
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.