ArticleMolecular biology of the cell2009
Competitive nuclear export of cyclin D1 and Hic-5 regulates anchorage dependence of cell growth and survival.
Article in Molecular biology of the cell, 2009. 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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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- The nuclear export protein exportin-1 in solid malignant tumours: From biology to clinical trials.Clinical and translational medicine · 2024Review
- Paxillin regulated genomic networks in prostate cancer.Steroids · 2019Article
- Regulation of mitochondrial ROS production by HIC-5: a common feature of oncogene-induced senescence and tumor invasiveness?The FEBS journal · 2019Article
- A mitochondrial ROS pathway controls matrix metalloproteinase 9 levels and invasive properties in RAS-activated cancer cells.The FEBS journal · 2019Article
- Pharmacological treatment with inhibitors of nuclear export enhances the antitumor activity of docetaxel in human prostate cancer.Oncotarget · 2017Article
- Dual PI3K/mTOR inhibitor, XL765 (SAR245409), shows superior effects to sole PI3K [XL147 (SAR245408)] or mTOR [rapamycin] inhibition in prostate cancer cell models.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- ANP32B is a nuclear target of henipavirus M proteins.PloS one · 2014Article
- A HIC-5- and KLF4-dependent mechanism transactivates p21(Cip1) in response to anchorage loss.The Journal of biological chemistry · 2012Article
- Hic-5 controls BMP4 responses in prostate cancer cells through interacting with Smads 1, 5 and 8.Oncogene · 2012Article
- Diverse roles for the paxillin family of proteins in cancer.Genes & cancer · 2012Article
- HIC-5: A Mobile Molecular Scaffold Regulating the Anchorage Dependence of Cell Growth.International journal of cell biology · 2012Article
- Expression of focal adhesion proteins in the developing rat kidney.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2011Article
- Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.Cell cycle (Georgetown, Tex.) · 2011Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anchorage dependence of cell growth and survival is a critical trait that distinguishes nontransformed cells from transformed cells. We demonstrate that anchorage dependence is determined by anchorage-dependent nuclear retention of cyclin D1, which is regulated by the focal adhesion protein, Hic-5, whose CRM1-dependent nuclear export counteracts that of cyclin D1. An adaptor protein, PINCH, interacts with cyclin D1 and Hic-5 and potentially serves as an interface for the competition between cyclin D1 and Hic-5 for CRM1. In nonadherent cells, the nuclear export of Hic-5, which is redox-sensitive, was interrupted due to elevated production of reactive oxygen species, and cyclin D1 was exported from the nucleus. When an Hic-5 mutant that was continuously exported in a reactive oxygen species-insensitive manner was introduced into the cells, cyclin D1 was retained in the nucleus under nonadherent conditions, and a significant population of cells escaped from growth arrest or apoptosis. Interestingly, activated ras achieved predominant cyclin D1 nuclear localization and thus, growth in nonadherent cells. We report a failsafe system for anchorage dependence of cell growth and survival.
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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.