Promoter of lncRNA Gene PVT1 Is a Tumor-Suppressor DNA Boundary Element
Open accessAbstract
Noncoding mutations in cancer genomes are frequent but challenging to interpret. PVT1 encodes an oncogenic lncRNA, but recurrent translocations and deletions in human cancers suggest alternative mechanisms. Here, we show that the PVT1 promoter has a tumor-suppressor function that is independent of PVT1 lncRNA. CRISPR interference of PVT1 promoter enhances breast cancer cell competition and growth in vivo. The promoters of the PVT1 and the MYC oncogenes, located 55 kb apart on chromosome 8q24, compete for engagement with four intragenic enhancers in the PVT1 locus, thereby allowing the PVT1 promoter to regulate pause release of MYC transcription. PVT1 undergoes developmentally regulated monoallelic expression, and the PVT1 promoter inhibits MYC expression only from the same chromosome via promoter competition. Cancer genome sequencing identifies recurrent mutations encompassing the human PVT1 promoter, and genome editing verified that PVT1 promoter mutation promotes cancer cell growth. These results highlight regulatory sequences of lncRNA genes as potential disease-associated DNA elements.
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Enhancers may have complex relationships with promoters, including feedback loops or competition with neighbouring genes.
“Enhancers may have complex relationships with promoters, including feedback loops or competition with neighbouring genes121,122.”
From Towards a comprehensive catalogue of validated and target-linked human enhancers (2020) · cites this paper as [121]
The Results section reports that PVT1 enhancers preferentially contact the PVT1 promoter, but shift toward the neighbouring MYC promoter when PVT1 is silenced; the Discussion describes this as promoter competition. Our copy does not describe feedback loops between enhancers and promoters, so it supports only the competition part of the claim. No page number is available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMPRAs would fail to recapitulate complex gene-enhancer networks.
“Finally, MPRAs would fail to recapitulate complex gene–enhancer networks121,122.”
From Towards a comprehensive catalogue of validated and target-linked human enhancers (2020) · cites this paper as [121]
The Results section describes a complex network in which PVT1 enhancers change their contacts with the PVT1 and MYC promoters. The paper does not say that MPRAs fail to recapitulate such networks; searches for MPRA and massively parallel reporter assays found no passage addressing that limitation. Page numbers were not available in our copy. (LLM, conf=0.80)
Experimental — accuracy not yet measuredEnhancers E1-E4 control expression of the PVT1 long noncoding RNA.
“Finally, we explored the potential utility of CRISPRoff for silencing promoter-distal elements by targeting enhancers that control the expression of the PVT1 long noncoding RNA (Cho et al., 2018; Fulco et al., 2016).”
From Genome-wide programmable transcriptional memory by CRISPR-based epigenome editing (2021) · cites this paper as Cho et al., 2018
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- Authors
- Cho, S. W., Xu, J., Sun, R., Mumbach, M. R., Carter, A. C., Chen, Y. G., Yost, K. E., Kim, J., He, J., Nevins, S. A., Chin, S.-F., Caldas, C., Liu, S. J., Horlbeck, M. A., Lim, D. A., Weissman, J. S., Curtis, C., & Chang, H. Y.
- Affiliations
- Stanford University (US)
- Stanford Medicine (US)
- Stanford Cancer Institute (US)
- University of Cambridge (GB)
- University of California, San Francisco (US)
- Howard Hughes Medical Institute (US)
- San Francisco VA Medical Center (US)
- Corresponding author
- Chang, Howard Y.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2018-05
- Volume
- 173
- Issue
- 6
- Pages
- 1398-1412.e22
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC5984165
- OpenAlex
- W2800290862
- Cited by
- 459
- References
- 17
- Citations by year
- 2026: 26 · 2025: 41 · 2024: 38 · 2023: 61 · 2022: 56 · 2021: 79 · 2020: 76 · 2019: 57 · 2018: 24
- FWCI
- 17.91
- Type
- journal article
- Language
- en
- Update notices
- erratum (2026-10-21)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Scholarworks@UNIST (Ulsan National Institute of Science and Technology) (submittedVersion)
- Funders
- Transgenic, Knockout, and Tumor Model Center of Stanford Cancer Institute
- NIH (R35-CA209919, P50-HG007735, 1R01- NS091544, R21-NS101395, U01-CA217882, R01-DA036858, S10OD018220)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- PVT1, long non-coding RNA, tumor suppressor function, MYC oncogene, promoter competition, monoallelic expression, pause release, transcriptional regulation, chromosome 8q24, non-coding mutations, breast cancer, CRISPR interference, cancer cell growth
- MeSH terms
- Animals, Breast Neoplasms, Cell Transformation, Neoplastic, Chromatin, DNA, Neoplasm, Enhancer Elements, Genetic, Female, Humans, Mutation, Neoplasm Transplantation, Promoter Regions, Genetic, Transcription, Genetic, Gene Expression Regulation, Neoplastic, Genes, myc, Mice, Inbred NOD, Gene Expression Profiling, Cell Line, Tumor, Cell Proliferation, Mice, RNA, Long Noncoding, Carcinogenesis, CRISPR-Cas Systems
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