ArticleThe Journal of clinical investigation2010
FAVL elevation in human tumors disrupts Fanconi anemia pathway signaling and promotes genomic instability and tumor growth.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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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.
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Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021Review
- Article
- A new look at molecular biology of breast cancer.Cancer biology & therapy · 2019Review
- Article
- Multifaceted Fanconi Anemia Signaling.Trends in genetics : TIG · 2018Review
- DNA methylation at the vicinity of the proximal polyadenylation site in FANCD2 gene involves human malignancy.Cell cycle (Georgetown, Tex.) · 2018Article
- Fanconi Anemia Signaling and Cancer.Trends in cancer · 2017Review
- Involvement of FANCD2 in Energy Metabolism via ATP5α.Scientific reports · 2017Article
- Overlooked FANCD2 variant encodes a promising, portent tumor suppressor, and alternative polyadenylation contributes to its expression.Oncotarget · 2017Article
- Fanconi Anemia Group D2 Protein Participates in Replication Origin Firing.Chemotherapy · 2016Article
- Article
- BLM promotes the activation of Fanconi Anemia signaling pathway.Oncotarget · 2016Article
- Distinct Metabolic Signature of Human Bladder Cancer Cells Carrying an Impaired Fanconi Anemia Tumor-Suppressor Signaling Pathway.Journal of proteome research · 2016Article
- Mutated Fanconi anemia pathway in non-Fanconi anemia cancers.Oncotarget · 2015Article
- Basal level of FANCD2 monoubiquitination is required for the maintenance of a sufficient number of licensed-replication origins to fire at a normal rate.Oncotarget · 2014Article
- Advances in the understanding of the Fanconi anemia tumor suppressor pathway.Cancer biology & therapy · 2013Review
- In vitro FANCD2 monoubiquitination by HHR6 and hRad18.Cell cycle (Georgetown, Tex.) · 2013Article
- Inhibitory effects of marine-derived DNA-binding anti-tumour tetrahydroisoquinolines on the Fanconi anaemia pathway.British journal of pharmacology · 2013Article
- A hidden role of the inactivated FANCD2: upregulating ΔNp63.Oncotarget · 2013Article
- Recruitment of DNA polymerase eta by FANCD2 in the early response to DNA damage.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a rare human genetic disease caused by mutations in any one of 13 known genes that encode proteins functioning in one common signaling pathway, the FA pathway, or in unknown genes. One characteristic of FA is an extremely high incidence of cancer, indicating the importance of the FA pathway in tumor suppression. However, the role of this pathway in the development and progression of human cancers in individuals who do not have FA has not been clearly determined. Here, we report that elevated expression of what we believe to be a novel splice variant of FA complementation group L (FANCL), which we identified and named FAVL, can impair the FA pathway in non-FA human tumor cells and act as a tumor promoting factor. FAVL expression was elevated in half of the human carcinoma cell lines and carcinoma tissue samples tested. Expression of FAVL resulted in decreased FANCL expression by sequestering FANCL to the cytoplasm and enhancing its degradation. Importantly, this impairment of the FA pathway by FAVL elevation provided human cancer cells with a growth advantage, caused chromosomal instability in vitro, and promoted tumor development in a xenograft mouse model. These data indicate that FAVL impairment of the FA pathway likely contributes to the development of non-FA human cancers and therefore add a challenging layer of complexity to the pathogenesis of human cancer. We further believe that these data will prove useful for developing additional tools for fighting human cancer.
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