ArticleCancer biology & therapy2013
Chromosomal structural variations during progression of a prostate epithelial cell line to a malignant metastatic state inactivate the NF2, NIPSNAP1, UGT2B17, and LPIN2 genes.
Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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
13 citing papers in PubMed, 18 citations in OpenAlex.
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- Comprehensive Analysis Reveals USP45 as a Novel Putative Oncogene in Pan-Cancer.Frontiers in molecular biosciences · 2022Article
- Knockdown of GBAS regulates esophageal cancer cell viability and apoptosis.Molecular medicine reports · 2021Article
- NIPSNAP protein family emerges as a sensor of mitochondrial health.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021Review
- NF2 Inhibits Proliferation and Cancer Stemness in Breast Cancer.Open medicine (Warsaw, Poland) · 2020Article
- MicroRNA‑92a promotes cell proliferation, migration and survival by directly targeting the tumor suppressor gene NF2 in colorectal and lung cancer cells.Oncology reports · 2019Article
- Downregulation of GBAS regulates oral squamous cell carcinoma proliferation and apoptosis via the p53 signaling pathway.OncoTargets and therapy · 2019Article
- Molecular Targets of Epigallocatechin-Gallate (EGCG): A Special Focus on Signal Transduction and Cancer.Nutrients · 2018Review
- Genome-Based Classification and Therapy of Prostate Cancer.Diagnostics (Basel, Switzerland) · 2018Review
- Identification of large rearrangements in cancer genomes with barcode linked reads.Nucleic acids research · 2018Article
- Prediction of Chromatin Accessibility in Gene-Regulatory Regions from Transcriptomics Data.Scientific reports · 2017Article
- Immune-associated proteins with potentialOncology letters · 2016Article
- Role of Merlin/NF2 inactivation in tumor biology.Oncogene · 2016Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Prostate cancer is the second highest cause of male cancer deaths in the United States. A significant number of tumors advance to a highly invasive and metastatic stage, which is typically resistant to traditional cancer therapeutics. In order to identify chromosomal structural variants that may contribute to prostate cancer progression we sequenced the genomes of a HPV-18 immortalized nonmalignant human prostate epithelial cell line, RWPE1, and compared it to its malignant, metastatic derivative, WPE1-NB26. There were a total of 34 large (> 1 Mbp) and 38 small copy number variants (<100 kbp) in WPE1-NB26 that were not present in the precursor cell line. We also identified and validated 46 structural variants present in the two cell lines, of which 23 were unique to WPE1-NB26. Structural variants unique to the malignant cell line inactivated: (1) the neurofibromin2 (NF2) gene, a known tumor suppressor; (2) its neighboring gene NIPSNAP1, another putative tumor suppressor that inhibits TRPV6, an anti-apoptotic oncogene implicated in prostate cancer progression; (3) UGT2B17, a gene that inactivates dihydrotestosterone, a known activator of prostate cancer progression; and (4) LPIN2, a phosphatidic acid phosphatase and a co-factor of PGC1a that is important for lipid metabolism and for suppressing autoinflammation. Our results illustrate the value of comparing the genomes of defined related pairs of cell lines to discover chromosomal structural variants that may contribute to cancer progression.
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