Hypoxia inducible factor-1a-dependent epithelial to mesenchymal transition under hypoxic conditions in prostate cancer cells

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
Yongguang Jiang (Creator)
Qing Li (Creator)
Mingchuan Li (Creator)
Yong Luo (Creator)
Yong Xing Wang (Creator)
Jiao Zhang (Creator)
Jiahui Zhao (Creator)
Institution
East Carolina University (ECU )
Web Site: http://www.ecu.edu/lib/

Abstract: Prostate cancer is the most commonly diagnosed\r\ncancer in men and the second leading cause of cancer death.\r\nHypoxia is an environmental stimulus that plays an important\r\nrole in the development and cancer progression especially for\r\nsolid tumors. The key regulator under hypoxic conditions is\r\nstabilized hypoxia-inducible factor (HIF)-1a. In the present\r\nstudy, immune-fluorescent staining, siRNAs, qRT-PC, immunoblotting, cell migration and invasion assays were carried\r\nout to test typical epithelial to mesenchymal transition under\r\nhypoxia and the key regulators of this process in PC3, a human\r\nprostate cancer cell line. Our data demonstrated that hypoxia\r\ninduces diverse molecular, phenotypic and functional changes\r\nin prostate cancer cells that are consistent with EMT. We\r\nalso showed that a cell signal factor such as HIF-1a, which\r\nmight be stabilized under hypoxic environment, is involved in\r\nEMT and cancer cell invasive potency. The induced hypoxia\r\ncould be blocked by HIF-1a gene silencing and reoxygenation\r\nof EMT in prostate cancer cells, hypoxia partially reversed\r\naccompanied by a process of mesenchymal-epithelial reverting\r\ntransition (MErT). EMT might be induced by activation of\r\nHIF-1a-dependent cell signaling in hypoxic prostate cancer\r\ncells.

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Publication
Other
Language: English
Date: 2023

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Hypoxia inducible factor-1a-dependent epithelial to mesenchymal transition under hypoxic conditions in prostate cancer cellshttp://hdl.handle.net/10342/8200The described resource references, cites, or otherwise points to the related resource.