ArticleCancer gene therapy2008
Adenovirus-mediated restoration of expression of the tumor suppressor gene DLC1 inhibits the proliferation and tumorigenicity of aggressive, androgen-independent human prostate cancer cell lines: prospects for gene therapy.
Article in Cancer gene therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Aqueous Humor Markers in Retinoblastoma, a Review.Translational vision science & technology · 2019Review
- Cooperative antiproliferative effect of coordinated ectopic expression of DLC1 tumor suppressor protein and silencing of MYC oncogene expression in liver cancer cells: Therapeutic implications.Oncology letters · 2016Article
- Dlc1 interaction with non-muscle myosin heavy chain II-A (Myh9) and Rac1 activation.Biology open · 2016Article
- Article
- Deleted in liver cancer-1 (DLC1): an emerging metastasis suppressor gene.Molecular diagnosis & therapy · 2014Review
- DLC1 induces expression of E-cadherin in prostate cancer cells through Rho pathway and suppresses invasion.Oncogene · 2014Article
- DLC1 suppresses NF-κB activity in prostate cancer cells due to its stabilizing effect on adherens junctions.SpringerPlus · 2014Article
- Uncovering the rare variants of DLC1 isoform 1 and their functional effects in a Chinese sporadic congenital heart disease cohort.PloS one · 2014Article
- DLC1 as a regulator of proliferation, invasion, cell cycle, and apoptosis in cutaneous squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Role of DLC1 tumor suppressor gene and MYC oncogene in pathogenesis of human hepatocellular carcinoma: potential prospects for combined targeted therapeutics (review).International journal of oncology · 2012Review
- DLC1 interaction with α-catenin stabilizes adherens junctions and enhances DLC1 antioncogenic activity.Molecular and cellular biology · 2012Article
- Preclinical evaluation of combined antineoplastic effect of DLC1 tumor suppressor protein and suberoylanilide hydroxamic acid on prostate cancer cells.Biochemical and biophysical research communications · 2012Article
- Detection and Clinical Significance of DLC1 Gene Methylation in Serum DNA from Colorectal Cancer Patients.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2011Article
- DLC1 interaction with S100A10 mediates inhibition of in vitro cell invasion and tumorigenicity of lung cancer cells through a RhoGAP-independent mechanism.Cancer research · 2011Article
- A pathogenic relationship between a regulator of the actin cytoskeleton and serum response factor.Genetics · 2010Article
- p120Ras-GAP binds the DLC1 Rho-GAP tumor suppressor protein and inhibits its RhoA GTPase and growth-suppressing activities.Oncogene · 2009Article
- DLC1 tumor suppressor gene inhibits migration and invasion of multiple myeloma cells through RhoA GTPase pathway.Leukemia · 2009Article
- DLC1: a significant GAP in the cancer genome.Genes & development · 2008Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Our recent study showing highly recurrent loss of function of DLC1 (deleted in liver cancer 1), a tumor suppressor gene in primary prostate carcinoma (PCA), implicates this gene in the pathogenesis of this disease. To evaluate the response of PCA to oncosuppressive activity of DLC1, we examined now the effects of adenoviral vector for human DLC1 transduction into the DLC1-deficient, androgen-independent (AI) and aggressive human PCA cell lines PC-3 and C4-2-B2. Adenovirus-mediated restoration of DLC1 expression inhibited the proliferation, invasiveness and anchorage-independent growth of PC-3 and C4-2-B2 cells in vitro as well as the tumorigenicity of PC-3 cells in nude mice. It also induced cell-cycle arrest, inhibited the activation of RhoA and the formation of actin stress fibers. DLC1 induced apoptosis in C4-2-B2 cells, whereas it did not elicit such an effect in PC-3 cells. The abundance of the antiapoptotic protein Bcl-2 was greater in PC-3 cells than in C4-2-B2 cells, and PC-3 cells were rendered sensitive to DLC1-induced apoptosis by treatment with the Bcl-2 inhibitor HA14-1. These results suggest that adenovirus-mediated DLC1 transfer, alone or together with other agents, such as inhibitors of Bcl-2 or histone deacetylase, might prove effective in the treatment of aggressive, AI-PCA.
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