Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines.

2.50
HDL Handle:
http://hdl.handle.net/10033/134762
Title:
Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines.
Authors:
Emadi Baygi, Modjtaba; Soheili, Zahra Soheila; Schmitz, Ingo; Sameie, Shahram; Schulz, Wolfgang A
Abstract:
The epithelial-mesenchymal transition (EMT) is regarded as an important step in cancer metastasis. Snail, a master regulator of EMT, has been recently proposed to act additionally as a cell survival factor and inducer of motility. We have investigated the function of Snail (SNAI1) in prostate cancer cells by downregulating its expression via short (21-mer) interfering RNA (siRNA) and measuring the consequences on EMT markers, cell viability, death, cell cycle, senescence, attachment, and invasivity. Of eight carcinoma cell lines, the prostate carcinoma cell lines LNCaP and PC-3 showed the highest and moderate expression of SNAI1 mRNA, respectively, as measured by quantitative RT-PCR. Long-term knockdown of Snail induced a severe decline in cell numbers in LNCaP and PC-3 and caspase activity was accordingly enhanced in both cell lines. In addition, suppression of Snail expression induced senescence in LNCaP cells. SNAI1-siRNA-treated cells did not tolerate detachment from the extracellular matrix, probably due to downregulation of integrin α6. Expression of E-cadherin, vimentin, and fibronectin was also affected. Invasiveness of PC-3 cells was not significantly diminished by Snail knockdown. Our data suggest that Snail acts primarily as a survival factor and inhibitor of cellular senescence in prostate cancer cell lines. We therefore propose that Snail can act as early driver of prostate cancer progression.
Affiliation:
Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Citation:
Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines. 2010, 26 (6):553-67 Cell Biol. Toxicol.
Journal:
Cell biology and toxicology
Issue Date:
Dec-2010
URI:
http://hdl.handle.net/10033/134762
DOI:
10.1007/s10565-010-9163-5
PubMed ID:
20397042
Type:
Article
Language:
en
ISSN:
1573-6822
Appears in Collections:
Publications of RG Signalling and Motility (SIM)

Full metadata record

DC FieldValueLanguage
dc.contributor.authorEmadi Baygi, Modjtabaen
dc.contributor.authorSoheili, Zahra Soheilaen
dc.contributor.authorSchmitz, Ingoen
dc.contributor.authorSameie, Shahramen
dc.contributor.authorSchulz, Wolfgang Aen
dc.date.accessioned2011-06-28T13:47:38Z-
dc.date.available2011-06-28T13:47:38Z-
dc.date.issued2010-12-
dc.identifier.citationSnail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines. 2010, 26 (6):553-67 Cell Biol. Toxicol.en
dc.identifier.issn1573-6822-
dc.identifier.pmid20397042-
dc.identifier.doi10.1007/s10565-010-9163-5-
dc.identifier.urihttp://hdl.handle.net/10033/134762-
dc.description.abstractThe epithelial-mesenchymal transition (EMT) is regarded as an important step in cancer metastasis. Snail, a master regulator of EMT, has been recently proposed to act additionally as a cell survival factor and inducer of motility. We have investigated the function of Snail (SNAI1) in prostate cancer cells by downregulating its expression via short (21-mer) interfering RNA (siRNA) and measuring the consequences on EMT markers, cell viability, death, cell cycle, senescence, attachment, and invasivity. Of eight carcinoma cell lines, the prostate carcinoma cell lines LNCaP and PC-3 showed the highest and moderate expression of SNAI1 mRNA, respectively, as measured by quantitative RT-PCR. Long-term knockdown of Snail induced a severe decline in cell numbers in LNCaP and PC-3 and caspase activity was accordingly enhanced in both cell lines. In addition, suppression of Snail expression induced senescence in LNCaP cells. SNAI1-siRNA-treated cells did not tolerate detachment from the extracellular matrix, probably due to downregulation of integrin α6. Expression of E-cadherin, vimentin, and fibronectin was also affected. Invasiveness of PC-3 cells was not significantly diminished by Snail knockdown. Our data suggest that Snail acts primarily as a survival factor and inhibitor of cellular senescence in prostate cancer cell lines. We therefore propose that Snail can act as early driver of prostate cancer progression.en
dc.language.isoenen
dc.subject.meshCell Agingen
dc.subject.meshCell Line, Tumoren
dc.subject.meshCell Survivalen
dc.subject.meshDown-Regulationen
dc.subject.meshEpithelial-Mesenchymal Transitionen
dc.subject.meshGene Expression Regulation, Neoplasticen
dc.subject.meshHumansen
dc.subject.meshIntegrin alpha6en
dc.subject.meshMaleen
dc.subject.meshNeoplasm Metastasisen
dc.subject.meshProstatic Neoplasmsen
dc.subject.meshRNA, Messengeren
dc.subject.meshTranscription Factorsen
dc.titleSnail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines.en
dc.typeArticleen
dc.contributor.departmentDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.en
dc.identifier.journalCell biology and toxicologyen

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