Involvement of c-Src/STAT3 signal in EGF-induced proliferation of rat spermatogonial stem cells
Epidermal growth factor (EGF) plays a role in male germ cell development, but the precise function is yet to be defined. This study shows that EGF stimulates rat spermatogonial proliferation in a dose-dependent manner and significantly increased the protein levels of phosphated c-Src (p-c-Src) and p...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2011-12, Vol.358 (1-2), p.67-73 |
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| creator | Chen, Jia-Xiang Xu, Lin-Lin Wang, Xin-Chang Qin, Hai-Yan Wang, Jing-Lei |
| description | Epidermal growth factor (EGF) plays a role in male germ cell development, but the precise function is yet to be defined. This study shows that EGF stimulates rat spermatogonial proliferation in a dose-dependent manner and significantly increased the protein levels of phosphated c-Src (p-c-Src) and phosphated signal transducer and activator of transcription 3 (p-STAT3). Moreover, overexpression of c-Src tagged with enhanced green fluorescence protein (EGFP) in rat spermatogonial stem cells enhances the cell viability. In contrast, knockdown or inhibition of c-Src inhibits rat spermatogonial stem cell proliferation; EGF could not abrogate the inhibitory effect. Evidently, the content of p-STAT3 protein was increased in c-Src-expressing cells and decreased in c-Src-suppressing cells. Furthermore, knockdown or inhibition of STAT3 also suppressed cell viability; neither EGF nor increased c-Src could reverse the inhibitory effect. These results are the first evidence that EGF induces proliferation of rat spermatogonial stem cells through c-Src/STAT3 signal. |
| doi_str_mv | 10.1007/s11010-011-0922-2 |
| format | Article |
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This study shows that EGF stimulates rat spermatogonial proliferation in a dose-dependent manner and significantly increased the protein levels of phosphated c-Src (p-c-Src) and phosphated signal transducer and activator of transcription 3 (p-STAT3). Moreover, overexpression of c-Src tagged with enhanced green fluorescence protein (EGFP) in rat spermatogonial stem cells enhances the cell viability. In contrast, knockdown or inhibition of c-Src inhibits rat spermatogonial stem cell proliferation; EGF could not abrogate the inhibitory effect. Evidently, the content of p-STAT3 protein was increased in c-Src-expressing cells and decreased in c-Src-suppressing cells. Furthermore, knockdown or inhibition of STAT3 also suppressed cell viability; neither EGF nor increased c-Src could reverse the inhibitory effect. These results are the first evidence that EGF induces proliferation of rat spermatogonial stem cells through c-Src/STAT3 signal.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-011-0922-2</identifier><identifier>PMID: 21678081</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cellular biology ; Epidermal growth factor ; Epidermal Growth Factor - pharmacology ; Fluorescence ; Humans ; Indexing in process ; Life Sciences ; Male ; Medical Biochemistry ; Oncology ; Phosphorylation - drug effects ; Protein-Tyrosine Kinases - metabolism ; Proteins ; Rats ; Rodents ; Signal Transduction - drug effects ; Spermatogonia - cytology ; src-Family Kinases ; STAT3 Transcription Factor - antagonists & inhibitors ; STAT3 Transcription Factor - metabolism ; Stem cells ; Stem Cells - cytology ; Stem Cells - drug effects ; Stem Cells - enzymology</subject><ispartof>Molecular and cellular biochemistry, 2011-12, Vol.358 (1-2), p.67-73</ispartof><rights>Springer Science+Business Media, LLC. 2011</rights><rights>COPYRIGHT 2011 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-eda6c2e9952e1d8e9a9b066959fce4331949b42378eea45771bd64c5623c160d3</citedby><cites>FETCH-LOGICAL-c508t-eda6c2e9952e1d8e9a9b066959fce4331949b42378eea45771bd64c5623c160d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-011-0922-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-011-0922-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21678081$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Jia-Xiang</creatorcontrib><creatorcontrib>Xu, Lin-Lin</creatorcontrib><creatorcontrib>Wang, Xin-Chang</creatorcontrib><creatorcontrib>Qin, Hai-Yan</creatorcontrib><creatorcontrib>Wang, Jing-Lei</creatorcontrib><title>Involvement of c-Src/STAT3 signal in EGF-induced proliferation of rat spermatogonial stem cells</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Epidermal growth factor (EGF) plays a role in male germ cell development, but the precise function is yet to be defined. This study shows that EGF stimulates rat spermatogonial proliferation in a dose-dependent manner and significantly increased the protein levels of phosphated c-Src (p-c-Src) and phosphated signal transducer and activator of transcription 3 (p-STAT3). Moreover, overexpression of c-Src tagged with enhanced green fluorescence protein (EGFP) in rat spermatogonial stem cells enhances the cell viability. In contrast, knockdown or inhibition of c-Src inhibits rat spermatogonial stem cell proliferation; EGF could not abrogate the inhibitory effect. Evidently, the content of p-STAT3 protein was increased in c-Src-expressing cells and decreased in c-Src-suppressing cells. Furthermore, knockdown or inhibition of STAT3 also suppressed cell viability; neither EGF nor increased c-Src could reverse the inhibitory effect. These results are the first evidence that EGF induces proliferation of rat spermatogonial stem cells through c-Src/STAT3 signal.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cellular biology</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>Fluorescence</subject><subject>Humans</subject><subject>Indexing in process</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Oncology</subject><subject>Phosphorylation - drug effects</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Spermatogonia - cytology</subject><subject>src-Family Kinases</subject><subject>STAT3 Transcription Factor - antagonists & inhibitors</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - enzymology</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUFrHSEUhaW0JK9pfkA3Zegm3Zh4dRzH5SMkaSDQRV7X4nPuPAwz-qozgf77OkyaQqHFhXL9zuHoIeQjsEtgTF1lAAaMMgDKNOeUvyEbkErQWoN-SzZMMEZbUOqUvM_5iRW4sCfklEOjWtbChpj78ByHZxwxTFXsK0cfk7t63G13osr-EOxQ-VDd3N1SH7rZYVcdUxx8j8lOPoZFUk5VPmIa7RQPMfgiyROOlcNhyB_Iu94OGc9f9jPy_fZmd_2VPny7u7_ePlAnWTtR7GzjOGotOULXorZ6z5pGS907rIUAXet9zYVqEW0tlYJ919RONlw4aFgnzsjF6lvi_ZgxT2b0eUlgA8Y5G728nStVF_LLf0kALnndtMAL-vkv9CnOqfzJ4sdKiNXvcoUOdkDjQx-nZF1ZHY7exYC9L_OtkLoGAAlFAKvApZhzwt4ckx9t-mmAmaVXs_ZqSldm6dUsST69JJn3I3avit9FFoCvQC5X4YDpT9R_u_4C6faqtA</recordid><startdate>20111201</startdate><enddate>20111201</enddate><creator>Chen, Jia-Xiang</creator><creator>Xu, Lin-Lin</creator><creator>Wang, Xin-Chang</creator><creator>Qin, Hai-Yan</creator><creator>Wang, Jing-Lei</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7QO</scope><scope>7X8</scope></search><sort><creationdate>20111201</creationdate><title>Involvement of c-Src/STAT3 signal in EGF-induced proliferation of rat spermatogonial stem cells</title><author>Chen, Jia-Xiang ; Xu, Lin-Lin ; Wang, Xin-Chang ; Qin, Hai-Yan ; Wang, Jing-Lei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-eda6c2e9952e1d8e9a9b066959fce4331949b42378eea45771bd64c5623c160d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cellular biology</topic><topic>Epidermal growth factor</topic><topic>Epidermal Growth Factor - pharmacology</topic><topic>Fluorescence</topic><topic>Humans</topic><topic>Indexing in process</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medical Biochemistry</topic><topic>Oncology</topic><topic>Phosphorylation - drug effects</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Spermatogonia - cytology</topic><topic>src-Family Kinases</topic><topic>STAT3 Transcription Factor - antagonists & inhibitors</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Stem cells</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - enzymology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Jia-Xiang</creatorcontrib><creatorcontrib>Xu, Lin-Lin</creatorcontrib><creatorcontrib>Wang, Xin-Chang</creatorcontrib><creatorcontrib>Qin, Hai-Yan</creatorcontrib><creatorcontrib>Wang, Jing-Lei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>Biotechnology Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Jia-Xiang</au><au>Xu, Lin-Lin</au><au>Wang, Xin-Chang</au><au>Qin, Hai-Yan</au><au>Wang, Jing-Lei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of c-Src/STAT3 signal in EGF-induced proliferation of rat spermatogonial stem cells</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2011-12-01</date><risdate>2011</risdate><volume>358</volume><issue>1-2</issue><spage>67</spage><epage>73</epage><pages>67-73</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Epidermal growth factor (EGF) plays a role in male germ cell development, but the precise function is yet to be defined. This study shows that EGF stimulates rat spermatogonial proliferation in a dose-dependent manner and significantly increased the protein levels of phosphated c-Src (p-c-Src) and phosphated signal transducer and activator of transcription 3 (p-STAT3). Moreover, overexpression of c-Src tagged with enhanced green fluorescence protein (EGFP) in rat spermatogonial stem cells enhances the cell viability. In contrast, knockdown or inhibition of c-Src inhibits rat spermatogonial stem cell proliferation; EGF could not abrogate the inhibitory effect. Evidently, the content of p-STAT3 protein was increased in c-Src-expressing cells and decreased in c-Src-suppressing cells. Furthermore, knockdown or inhibition of STAT3 also suppressed cell viability; neither EGF nor increased c-Src could reverse the inhibitory effect. These results are the first evidence that EGF induces proliferation of rat spermatogonial stem cells through c-Src/STAT3 signal.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21678081</pmid><doi>10.1007/s11010-011-0922-2</doi><tpages>7</tpages></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2011-12, Vol.358 (1-2), p.67-73 |
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| subjects | Animals Biochemistry Biomedical and Life Sciences Cardiology Cell Proliferation - drug effects Cell Survival - drug effects Cellular biology Epidermal growth factor Epidermal Growth Factor - pharmacology Fluorescence Humans Indexing in process Life Sciences Male Medical Biochemistry Oncology Phosphorylation - drug effects Protein-Tyrosine Kinases - metabolism Proteins Rats Rodents Signal Transduction - drug effects Spermatogonia - cytology src-Family Kinases STAT3 Transcription Factor - antagonists & inhibitors STAT3 Transcription Factor - metabolism Stem cells Stem Cells - cytology Stem Cells - drug effects Stem Cells - enzymology |
| title | Involvement of c-Src/STAT3 signal in EGF-induced proliferation of rat spermatogonial stem cells |
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