ArticleEpigenetics2011
Reactivation of MASPIN in non-small cell lung carcinoma (NSCLC) cells by artificial transcription factors (ATFs).
Article in Epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- LncRNA MRPL39 inhibits cell proliferation and migration by regulating miR-130/TSC1 axis in non-small cell lung cancer.3 Biotech · 2024Article
- Epigenetic reactivation of tumor suppressor genes with CRISPRa technologies as precision therapy for hepatocellular carcinoma.Clinical epigenetics · 2023Article
- CRISPR Technology in Cancer Diagnosis and Treatment: Opportunities and Challenges.Biochemical genetics · 2022Review
- Epigenetic Editing in Prostate Cancer: Challenges and Opportunities.Epigenetics · 2022Review
- Integrating the tumor-suppressive activity of Maspin with p53 in retuning the epithelial homeostasis: A working hypothesis and applicable prospects.Frontiers in oncology · 2022Review
- Reprogramming the anti-tumor immune response via CRISPR genetic and epigenetic editing.Molecular therapy. Methods & clinical development · 2021Review
- Tumour suppression by targeted intravenous non-viral CRISPRa using dendritic polymers.Chemical science · 2019Article
- Activating PTEN Tumor Suppressor Expression with the CRISPR/dCas9 System.Molecular therapy. Nucleic acids · 2019Article
- Epigenetic editing of the Dlg4/PSD95 gene improves cognition in aged and Alzheimer's disease mice.Brain : a journal of neurology · 2017Article
- Synthetically controlling dendrimer flexibility improves delivery of large plasmid DNA.Chemical science · 2017Article
- Waking up dormant tumor suppressor genes with zinc fingers, TALEs and the CRISPR/dCas9 system.Oncotarget · 2016Article
- Re-expression of Selected Epigenetically Silenced Candidate Tumor Suppressor Genes in Cervical Cancer by TET2-directed Demethylation.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Epigenome engineering in cancer: fairytale or a realistic path to the clinic?Frontiers in oncology · 2015Review
- Prolonged re-expression of the hypermethylated gene EPB41L3 using artificial transcription factors and epigenetic drugs.Epigenetics · 2015Article
- Expression and localization of maspin in cervical cancer and its role in tumor progression and lymphangiogenesis.Archives of gynecology and obstetrics · 2014Article
- Induced DNA demethylation by targeting Ten-Eleven Translocation 2 to the human ICAM-1 promoter.Nucleic acids research · 2014Article
- Analysis of an artificial zinc finger epigenetic modulator: widespread binding but limited regulation.Nucleic acids research · 2014Article
- Functional validation of putative tumor suppressor gene C13ORF18 in cervical cancer by Artificial Transcription Factors.Molecular oncology · 2013Article
- Role of maspin in cancer.Clinical and translational medicine · 2013Article
- Bidirectional modulation of endogenous EpCAM expression to unravel its function in ovarian cancer.British journal of cancer · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tumor suppressor genes have antiproliferative and antimetastatic functions, and thus, they negatively affect tumor progression. Reactivating specific tumor suppressor genes would offer an important therapeutic strategy to block tumor progression. Mammary Serine Protease Inhibitor (MASPIN) is a tumor suppressor gene that is not mutated or rearranged in tumor cells, but is silenced during metastatic progression by transcriptional and epigenetic mechanisms. In this work, we have investigated the ability of Artificial Transcription Factors (ATFs) to reactivate MASPIN expression and to reduce tumor growth and metastatic dissemination in Non-Small Cell Lung Carcinoma (NSCLC) cell lines carrying a hypermethylated MASPIN promoter. We found that the ATFs linked to transactivator domains were able to demethylate the MASPIN promoter. Consistently, we observed that co-treatment of ATF-transduced cells with methyltransferase inhibitors enhanced MASPIN expression as well as induction of tumor cell apoptosis. In addition to tumor suppressive functions, restoration of endogenous MASPIN expression was accompanied by inhibition of metastatic dissemination in nude mice. ATF-mediated reactivation of MASPIN lead to changes in cell motility and to induction of E-CADHERIN. These data suggest that ATFs are able to reprogram aggressive lung tumor cells towards a more epithelial, differentiated phenotype, and thus, represent novel therapeutic agents for metastatic lung cancers.
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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.