Cyclin A1, the alternative A-type cyclin, contributes to G1 S cell cycle progression in somatic cells
Cyclin A1 is an alternative A-type cyclin that is essential for spermatogenesis, but it is also expressed in hematopoietic progenitor cells and in acute myeloid leukemia. Its functions during cell cycle progression of somatic cells are incompletely understood. Here, we have analysed the cell cycle f...
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| Veröffentlicht in: | Oncogene 2005-04, Vol.24 (16), p.2739-2744 |
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| creator | PING JI AGRAWAL, Shuchi SERVE, Hubert MÜLLER-TIDOW, Carsten DIEDERICHS, Sven BÄUMER, Nicole BECKER, Annette CAUVET, Thomas KOWSKI, Sascha BEGER, Carmela WELTE, Karl BERDEL, Wolfgang E |
| description | Cyclin A1 is an alternative A-type cyclin that is essential for spermatogenesis, but it is also expressed in hematopoietic progenitor cells and in acute myeloid leukemia. Its functions during cell cycle progression of somatic cells are incompletely understood. Here, we have analysed the cell cycle functions of cyclin A1 in transformed and nontransformed cells. Murine embryonic fibroblasts derived from cyclin A1-deficient mice were significantly impaired in their proliferative capacity. In accordance, cyclin A1-/- cells accumulated in G1 and G2/M phase while the percentage of S phase cells decreased. Also, lectin stimulated splenic lymphocytes from cyclin A1-/- mice proliferated slower than their wild-type counterparts. Forced cyclin A1 overexpression in NIH3T3 cells and in U937 leukemic cells either by transient transfection or by retroviral infection enhanced S phase entry. Consequently, siRNA mediated silencing of cyclin A1 in highly cyclin A1 expressing ML1 leukemic cells significantly slowed S phase entry, decreased proliferation and inhibited colony formation. Taken together, these analyses demonstrate that cyclin A1 contributes to G1 to S cell cycle progression in somatic cells. Cyclin A1 overexpression enhances S phase entry consistent with an oncogenic function. Finally, cyclin A1 might be a therapeutic target since its silencing inhibited leukemia cell growth. |
| doi_str_mv | 10.1038/sj.onc.1208356 |
| format | Article |
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Its functions during cell cycle progression of somatic cells are incompletely understood. Here, we have analysed the cell cycle functions of cyclin A1 in transformed and nontransformed cells. Murine embryonic fibroblasts derived from cyclin A1-deficient mice were significantly impaired in their proliferative capacity. In accordance, cyclin A1-/- cells accumulated in G1 and G2/M phase while the percentage of S phase cells decreased. Also, lectin stimulated splenic lymphocytes from cyclin A1-/- mice proliferated slower than their wild-type counterparts. Forced cyclin A1 overexpression in NIH3T3 cells and in U937 leukemic cells either by transient transfection or by retroviral infection enhanced S phase entry. Consequently, siRNA mediated silencing of cyclin A1 in highly cyclin A1 expressing ML1 leukemic cells significantly slowed S phase entry, decreased proliferation and inhibited colony formation. Taken together, these analyses demonstrate that cyclin A1 contributes to G1 to S cell cycle progression in somatic cells. Cyclin A1 overexpression enhances S phase entry consistent with an oncogenic function. Finally, cyclin A1 might be a therapeutic target since its silencing inhibited leukemia cell growth.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1208356</identifier><identifier>PMID: 15829981</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Acute myeloid leukemia ; Animals ; Biological and medical sciences ; Cell cycle ; Cell physiology ; Cell Proliferation ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cell Transformation, Neoplastic ; Cyclin A - genetics ; Cyclin A - metabolism ; Cyclin A1 ; Embryo fibroblasts ; Female ; Fundamental and applied biological sciences. Psychology ; G1 Phase ; Gene Expression ; Hematologic and hematopoietic diseases ; Hematology ; Hematopoietic stem cells ; Humans ; Incorporation ; Kinetics ; Leukemia ; Leukemia - genetics ; Leukemia - metabolism ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphocytes ; Male ; Medical sciences ; Mice ; Mice, Knockout ; Molecular and cellular biology ; NIH 3T3 Cells ; Oligoribonucleotides ; Oncology ; Progenitor cells ; S Phase ; siRNA ; Somatic cells ; Spermatogenesis ; Spleen ; Therapeutic targets ; Transfection ; U937 Cells</subject><ispartof>Oncogene, 2005-04, Vol.24 (16), p.2739-2744</ispartof><rights>2005 INIST-CNRS</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 14, 2005</rights><rights>Nature Publishing Group 2005.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-bc1b41ba1c13a19a119add2b0aee92c1528319dd29358e7f88470d7b7d213b543</citedby><cites>FETCH-LOGICAL-c510t-bc1b41ba1c13a19a119add2b0aee92c1528319dd29358e7f88470d7b7d213b543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,2731,27933,27934</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16712850$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15829981$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PING JI</creatorcontrib><creatorcontrib>AGRAWAL, Shuchi</creatorcontrib><creatorcontrib>SERVE, Hubert</creatorcontrib><creatorcontrib>MÜLLER-TIDOW, Carsten</creatorcontrib><creatorcontrib>DIEDERICHS, Sven</creatorcontrib><creatorcontrib>BÄUMER, Nicole</creatorcontrib><creatorcontrib>BECKER, Annette</creatorcontrib><creatorcontrib>CAUVET, Thomas</creatorcontrib><creatorcontrib>KOWSKI, Sascha</creatorcontrib><creatorcontrib>BEGER, Carmela</creatorcontrib><creatorcontrib>WELTE, Karl</creatorcontrib><creatorcontrib>BERDEL, Wolfgang E</creatorcontrib><title>Cyclin A1, the alternative A-type cyclin, contributes to G1 S cell cycle progression in somatic cells</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Cyclin A1 is an alternative A-type cyclin that is essential for spermatogenesis, but it is also expressed in hematopoietic progenitor cells and in acute myeloid leukemia. Its functions during cell cycle progression of somatic cells are incompletely understood. Here, we have analysed the cell cycle functions of cyclin A1 in transformed and nontransformed cells. Murine embryonic fibroblasts derived from cyclin A1-deficient mice were significantly impaired in their proliferative capacity. In accordance, cyclin A1-/- cells accumulated in G1 and G2/M phase while the percentage of S phase cells decreased. Also, lectin stimulated splenic lymphocytes from cyclin A1-/- mice proliferated slower than their wild-type counterparts. Forced cyclin A1 overexpression in NIH3T3 cells and in U937 leukemic cells either by transient transfection or by retroviral infection enhanced S phase entry. Consequently, siRNA mediated silencing of cyclin A1 in highly cyclin A1 expressing ML1 leukemic cells significantly slowed S phase entry, decreased proliferation and inhibited colony formation. Taken together, these analyses demonstrate that cyclin A1 contributes to G1 to S cell cycle progression in somatic cells. Cyclin A1 overexpression enhances S phase entry consistent with an oncogenic function. Finally, cyclin A1 might be a therapeutic target since its silencing inhibited leukemia cell growth.</description><subject>Acute myeloid leukemia</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell cycle</subject><subject>Cell physiology</subject><subject>Cell Proliferation</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cyclin A - genetics</subject><subject>Cyclin A - metabolism</subject><subject>Cyclin A1</subject><subject>Embryo fibroblasts</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>G1 Phase</subject><subject>Gene Expression</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematology</subject><subject>Hematopoietic stem cells</subject><subject>Humans</subject><subject>Incorporation</subject><subject>Kinetics</subject><subject>Leukemia</subject><subject>Leukemia - genetics</subject><subject>Leukemia - metabolism</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphocytes</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Molecular and cellular biology</subject><subject>NIH 3T3 Cells</subject><subject>Oligoribonucleotides</subject><subject>Oncology</subject><subject>Progenitor cells</subject><subject>S Phase</subject><subject>siRNA</subject><subject>Somatic cells</subject><subject>Spermatogenesis</subject><subject>Spleen</subject><subject>Therapeutic targets</subject><subject>Transfection</subject><subject>U937 Cells</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0t2L1DAQAPAgireevvqmBEWfrmsmab4el0VP4cAH9Tmk6fTs0m3WpBX2vze3W1gQREIIDL9MhpkQ8hLYGpgwH_JuHcewBs6MkOoRWUGtVSWlrR-TFbOSVZYLfkWe5bxjjGnL-FNyBdJwaw2sCG6PYehHuoEbOv1E6ocJ0-in_jfSTTUdD0jDSdzQEMcp9c08YaZTpLdAv9GAw3ACSA8p3ifMuY8jLQlz3Jcs4STyc_Kk80PGF8t5TX58-vh9-7m6-3r7Zbu5q4IENlVNgKaGxkMA4cF6KLttecM8ouUBJDcCbIlYIQ3qzphas1Y3uuUgGlmLa_L-nLcU82vGPLl9nx8q8CPGOTultVBM_R-CNrXhCgp8-xfcxbk0aMiOqxpErYQURb35p-JaSGnAFLQ-o3s_oOvHLk7Jh7Ja3Peludj1Jb4BY5kGqfTlQkgx54SdO6R-79PRAXMP03d558r03TL9cuH1Usbc7LG98GXcBbxbgM_BD13yY-jzxSkN3EhW3KuzKz9hTngBy0N_AESWv0A</recordid><startdate>20050414</startdate><enddate>20050414</enddate><creator>PING JI</creator><creator>AGRAWAL, Shuchi</creator><creator>SERVE, Hubert</creator><creator>MÜLLER-TIDOW, Carsten</creator><creator>DIEDERICHS, Sven</creator><creator>BÄUMER, Nicole</creator><creator>BECKER, Annette</creator><creator>CAUVET, Thomas</creator><creator>KOWSKI, Sascha</creator><creator>BEGER, Carmela</creator><creator>WELTE, Karl</creator><creator>BERDEL, Wolfgang E</creator><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</scope><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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20050414</creationdate><title>Cyclin A1, the alternative A-type cyclin, contributes to G1 S cell cycle progression in somatic cells</title><author>PING JI ; AGRAWAL, Shuchi ; SERVE, Hubert ; MÜLLER-TIDOW, Carsten ; DIEDERICHS, Sven ; BÄUMER, Nicole ; BECKER, Annette ; CAUVET, Thomas ; KOWSKI, Sascha ; BEGER, Carmela ; WELTE, Karl ; BERDEL, Wolfgang E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-bc1b41ba1c13a19a119add2b0aee92c1528319dd29358e7f88470d7b7d213b543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acute myeloid leukemia</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell cycle</topic><topic>Cell physiology</topic><topic>Cell Proliferation</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cell Transformation, Neoplastic</topic><topic>Cyclin A - genetics</topic><topic>Cyclin A - metabolism</topic><topic>Cyclin A1</topic><topic>Embryo fibroblasts</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>G1 Phase</topic><topic>Gene Expression</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematology</topic><topic>Hematopoietic stem cells</topic><topic>Humans</topic><topic>Incorporation</topic><topic>Kinetics</topic><topic>Leukemia</topic><topic>Leukemia - genetics</topic><topic>Leukemia - metabolism</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. 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Its functions during cell cycle progression of somatic cells are incompletely understood. Here, we have analysed the cell cycle functions of cyclin A1 in transformed and nontransformed cells. Murine embryonic fibroblasts derived from cyclin A1-deficient mice were significantly impaired in their proliferative capacity. In accordance, cyclin A1-/- cells accumulated in G1 and G2/M phase while the percentage of S phase cells decreased. Also, lectin stimulated splenic lymphocytes from cyclin A1-/- mice proliferated slower than their wild-type counterparts. Forced cyclin A1 overexpression in NIH3T3 cells and in U937 leukemic cells either by transient transfection or by retroviral infection enhanced S phase entry. Consequently, siRNA mediated silencing of cyclin A1 in highly cyclin A1 expressing ML1 leukemic cells significantly slowed S phase entry, decreased proliferation and inhibited colony formation. 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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acute myeloid leukemia Animals Biological and medical sciences Cell cycle Cell physiology Cell Proliferation Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cell Transformation, Neoplastic Cyclin A - genetics Cyclin A - metabolism Cyclin A1 Embryo fibroblasts Female Fundamental and applied biological sciences. Psychology G1 Phase Gene Expression Hematologic and hematopoietic diseases Hematology Hematopoietic stem cells Humans Incorporation Kinetics Leukemia Leukemia - genetics Leukemia - metabolism Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphocytes Male Medical sciences Mice Mice, Knockout Molecular and cellular biology NIH 3T3 Cells Oligoribonucleotides Oncology Progenitor cells S Phase siRNA Somatic cells Spermatogenesis Spleen Therapeutic targets Transfection U937 Cells |
| title | Cyclin A1, the alternative A-type cyclin, contributes to G1 S cell cycle progression in somatic cells |
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