Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice
PTEN haploinsufficiency plays an important role in prostate cancer development in men. However, monoallelic deletion of Pten gene failed to induce high prostate intraepithelial neoplasia (PIN) until Pten+/− mice aged or fed a high-calorie diet. Because CEACAM1, a cell adhesion molecule with a potent...
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| creator | Liu, Jehnan Muturi, Harrison T. Khuder, Saja S. Helal, Raghd Abu Ghadieh, Hilda E. Ramakrishnan, Sadeesh K. Kaw, Meenakshi K. Lester, Sumona Ghosh Al-Khudhair, Ahmed Conran, Philip B. Chin, Khew-Voon Gatto-Weis, Cara Najjar, Sonia M. |
| description | PTEN haploinsufficiency plays an important role in prostate cancer development in men. However, monoallelic deletion of Pten gene failed to induce high prostate intraepithelial neoplasia (PIN) until Pten+/− mice aged or fed a high-calorie diet. Because CEACAM1, a cell adhesion molecule with a potential tumor suppression activity, is induced in Pten+/− prostates, the study aimed at examining whether the rise of CEACAM1 limited neoplastic progression in Pten+/− prostates.
Pten+/− were crossbred with Cc1−/− mice harboring a null deletion of Ceacam1 gene to produce Pten+/−/Cc1−/− double mutants. Prostates from 7-month old male mice were analyzed histologically and biochemically for PIN progression.
Deleting Ceacam1 in Pten+/− mice caused an early development of high-grade PIN in parallel to hyperactivation of PI3 kinase/Akt and Ras/MAP kinase pathways, with an increase in cell proliferation, epithelial-to-mesenchymal transition, angiogenesis and inflammation relative to Pten+/− and Cc1−/− individual mutants. It also caused a remarkable increase in lipogenesis in prostate despite maintaining insulin sensitivity. Concomitant Ceacam1 deletion with Pten+/− activated the IL-6/STAT3 signaling pathways to suppress Irf-8 transcription that in turn, led to a decrease in the expression level of promyelocytic leukemia gene, a well characterized tumor suppressor in prostate.
Ceacam1 deletion accelerated high-grade prostate intraepithelial neoplasia in Pten haploinsufficient mice while preserving insulin sensitivity. This demonstrated that the combined loss of Ceacam1 and Pten advanced prostate cancer by increasing lipogenesis and modifying the STAT3-dependent inflammatory microenvironment of prostate.
•CEACAM1-4L expression is elevated in prostates of Pten+/− mice.•Ceacam1 deletion causes progression of neoplasia in prostates of Pten+/− mice.•Ceacam1 deletion causes EMT and angiogenesis in prostates of Pten+/− mice.•Ceacam1 deletion causes lipogenesis and inflammation in prostates of Pten+/− mice.•Ceacam1 deletion activates STAT3 to limit Irf-8 and Pml transcription in Pten+/−. |
| doi_str_mv | 10.1016/j.metabol.2020.154215 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7283002</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0026049520300792</els_id><sourcerecordid>2383513532</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3825-25fca337e9093f5e69edff012d164919d954563e1aa54ba8319cb627deb8aa7a3</originalsourceid><addsrcrecordid>eNqFUU1r3DAQFaUh2aT5CS069uKtPizZvjSUpU0CC8khgd7EWB4lWmxrK3kX8u8js9uQnnrSaObNm8d7hHzmbMkZ1982ywEnaEO_FEzknioFVx_Igispiloz9pEsGBO6YGWjzsh5ShvGWFXV-pScSSFYIzVbkN_rkBINjq4QLAycbmMYwoRpLtIEE1ILo8U4_58ipuTDSP1I7ycc6TNs--DHtHPOW4_jRAfokQ7e4idy4qBPeHl8L8jjr58Pq5tifXd9u_qxLqyshSqEchakrLDJgpxC3WDnHOOi47pseNM1qlRaIgdQZQu15I1ttag6bGuACuQF-X7g3e7aATubRUTozTb6AeKLCeDNv5PRP5unsDeVqGU2KBN8PRLE8GeHaTKDTxb7HkYMu2SErKXiMtuaoeoAtdmbFNG9neHMzKmYjTmmYuZUzCGVvPflvca3rb8xZMDVAYDZqb3HaNJsp8XOR7ST6YL_z4lXd3miXg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2383513532</pqid></control><display><type>article</type><title>Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Liu, Jehnan ; Muturi, Harrison T. ; Khuder, Saja S. ; Helal, Raghd Abu ; Ghadieh, Hilda E. ; Ramakrishnan, Sadeesh K. ; Kaw, Meenakshi K. ; Lester, Sumona Ghosh ; Al-Khudhair, Ahmed ; Conran, Philip B. ; Chin, Khew-Voon ; Gatto-Weis, Cara ; Najjar, Sonia M.</creator><creatorcontrib>Liu, Jehnan ; Muturi, Harrison T. ; Khuder, Saja S. ; Helal, Raghd Abu ; Ghadieh, Hilda E. ; Ramakrishnan, Sadeesh K. ; Kaw, Meenakshi K. ; Lester, Sumona Ghosh ; Al-Khudhair, Ahmed ; Conran, Philip B. ; Chin, Khew-Voon ; Gatto-Weis, Cara ; Najjar, Sonia M.</creatorcontrib><description>PTEN haploinsufficiency plays an important role in prostate cancer development in men. However, monoallelic deletion of Pten gene failed to induce high prostate intraepithelial neoplasia (PIN) until Pten+/− mice aged or fed a high-calorie diet. Because CEACAM1, a cell adhesion molecule with a potential tumor suppression activity, is induced in Pten+/− prostates, the study aimed at examining whether the rise of CEACAM1 limited neoplastic progression in Pten+/− prostates.
Pten+/− were crossbred with Cc1−/− mice harboring a null deletion of Ceacam1 gene to produce Pten+/−/Cc1−/− double mutants. Prostates from 7-month old male mice were analyzed histologically and biochemically for PIN progression.
Deleting Ceacam1 in Pten+/− mice caused an early development of high-grade PIN in parallel to hyperactivation of PI3 kinase/Akt and Ras/MAP kinase pathways, with an increase in cell proliferation, epithelial-to-mesenchymal transition, angiogenesis and inflammation relative to Pten+/− and Cc1−/− individual mutants. It also caused a remarkable increase in lipogenesis in prostate despite maintaining insulin sensitivity. Concomitant Ceacam1 deletion with Pten+/− activated the IL-6/STAT3 signaling pathways to suppress Irf-8 transcription that in turn, led to a decrease in the expression level of promyelocytic leukemia gene, a well characterized tumor suppressor in prostate.
Ceacam1 deletion accelerated high-grade prostate intraepithelial neoplasia in Pten haploinsufficient mice while preserving insulin sensitivity. This demonstrated that the combined loss of Ceacam1 and Pten advanced prostate cancer by increasing lipogenesis and modifying the STAT3-dependent inflammatory microenvironment of prostate.
•CEACAM1-4L expression is elevated in prostates of Pten+/− mice.•Ceacam1 deletion causes progression of neoplasia in prostates of Pten+/− mice.•Ceacam1 deletion causes EMT and angiogenesis in prostates of Pten+/− mice.•Ceacam1 deletion causes lipogenesis and inflammation in prostates of Pten+/− mice.•Ceacam1 deletion activates STAT3 to limit Irf-8 and Pml transcription in Pten+/−.</description><identifier>ISSN: 0026-0495</identifier><identifier>ISSN: 1532-8600</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/j.metabol.2020.154215</identifier><identifier>PMID: 32209360</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Carcinoembryonic Antigen - genetics ; CEACAM1 ; Disease Progression ; Fatty acid synthase ; Haploinsufficiency ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Neoplasia ; Normoinsulinemia ; Oncogene Protein v-akt - genetics ; Phosphatidylinositol 3-Kinases - genetics ; PML ; Prostate intraepithelial neoplasia ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; PTEN Phosphohydrolase - genetics ; PTEN tumor suppression ; Signal Transduction - drug effects ; Signal Transduction - genetics ; STAT3 Transcription Factor - genetics</subject><ispartof>Metabolism, clinical and experimental, 2020-06, Vol.107, p.154215-154215, Article 154215</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3825-25fca337e9093f5e69edff012d164919d954563e1aa54ba8319cb627deb8aa7a3</citedby><cites>FETCH-LOGICAL-c3825-25fca337e9093f5e69edff012d164919d954563e1aa54ba8319cb627deb8aa7a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0026049520300792$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32209360$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Jehnan</creatorcontrib><creatorcontrib>Muturi, Harrison T.</creatorcontrib><creatorcontrib>Khuder, Saja S.</creatorcontrib><creatorcontrib>Helal, Raghd Abu</creatorcontrib><creatorcontrib>Ghadieh, Hilda E.</creatorcontrib><creatorcontrib>Ramakrishnan, Sadeesh K.</creatorcontrib><creatorcontrib>Kaw, Meenakshi K.</creatorcontrib><creatorcontrib>Lester, Sumona Ghosh</creatorcontrib><creatorcontrib>Al-Khudhair, Ahmed</creatorcontrib><creatorcontrib>Conran, Philip B.</creatorcontrib><creatorcontrib>Chin, Khew-Voon</creatorcontrib><creatorcontrib>Gatto-Weis, Cara</creatorcontrib><creatorcontrib>Najjar, Sonia M.</creatorcontrib><title>Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description>PTEN haploinsufficiency plays an important role in prostate cancer development in men. However, monoallelic deletion of Pten gene failed to induce high prostate intraepithelial neoplasia (PIN) until Pten+/− mice aged or fed a high-calorie diet. Because CEACAM1, a cell adhesion molecule with a potential tumor suppression activity, is induced in Pten+/− prostates, the study aimed at examining whether the rise of CEACAM1 limited neoplastic progression in Pten+/− prostates.
Pten+/− were crossbred with Cc1−/− mice harboring a null deletion of Ceacam1 gene to produce Pten+/−/Cc1−/− double mutants. Prostates from 7-month old male mice were analyzed histologically and biochemically for PIN progression.
Deleting Ceacam1 in Pten+/− mice caused an early development of high-grade PIN in parallel to hyperactivation of PI3 kinase/Akt and Ras/MAP kinase pathways, with an increase in cell proliferation, epithelial-to-mesenchymal transition, angiogenesis and inflammation relative to Pten+/− and Cc1−/− individual mutants. It also caused a remarkable increase in lipogenesis in prostate despite maintaining insulin sensitivity. Concomitant Ceacam1 deletion with Pten+/− activated the IL-6/STAT3 signaling pathways to suppress Irf-8 transcription that in turn, led to a decrease in the expression level of promyelocytic leukemia gene, a well characterized tumor suppressor in prostate.
Ceacam1 deletion accelerated high-grade prostate intraepithelial neoplasia in Pten haploinsufficient mice while preserving insulin sensitivity. This demonstrated that the combined loss of Ceacam1 and Pten advanced prostate cancer by increasing lipogenesis and modifying the STAT3-dependent inflammatory microenvironment of prostate.
•CEACAM1-4L expression is elevated in prostates of Pten+/− mice.•Ceacam1 deletion causes progression of neoplasia in prostates of Pten+/− mice.•Ceacam1 deletion causes EMT and angiogenesis in prostates of Pten+/− mice.•Ceacam1 deletion causes lipogenesis and inflammation in prostates of Pten+/− mice.•Ceacam1 deletion activates STAT3 to limit Irf-8 and Pml transcription in Pten+/−.</description><subject>Animals</subject><subject>Carcinoembryonic Antigen - genetics</subject><subject>CEACAM1</subject><subject>Disease Progression</subject><subject>Fatty acid synthase</subject><subject>Haploinsufficiency</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mutation</subject><subject>Neoplasia</subject><subject>Normoinsulinemia</subject><subject>Oncogene Protein v-akt - genetics</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>PML</subject><subject>Prostate intraepithelial neoplasia</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN tumor suppression</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>STAT3 Transcription Factor - genetics</subject><issn>0026-0495</issn><issn>1532-8600</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU1r3DAQFaUh2aT5CS069uKtPizZvjSUpU0CC8khgd7EWB4lWmxrK3kX8u8js9uQnnrSaObNm8d7hHzmbMkZ1982ywEnaEO_FEzknioFVx_Igispiloz9pEsGBO6YGWjzsh5ShvGWFXV-pScSSFYIzVbkN_rkBINjq4QLAycbmMYwoRpLtIEE1ILo8U4_58ipuTDSP1I7ycc6TNs--DHtHPOW4_jRAfokQ7e4idy4qBPeHl8L8jjr58Pq5tifXd9u_qxLqyshSqEchakrLDJgpxC3WDnHOOi47pseNM1qlRaIgdQZQu15I1ttag6bGuACuQF-X7g3e7aATubRUTozTb6AeKLCeDNv5PRP5unsDeVqGU2KBN8PRLE8GeHaTKDTxb7HkYMu2SErKXiMtuaoeoAtdmbFNG9neHMzKmYjTmmYuZUzCGVvPflvca3rb8xZMDVAYDZqb3HaNJsp8XOR7ST6YL_z4lXd3miXg</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Liu, Jehnan</creator><creator>Muturi, Harrison T.</creator><creator>Khuder, Saja S.</creator><creator>Helal, Raghd Abu</creator><creator>Ghadieh, Hilda E.</creator><creator>Ramakrishnan, Sadeesh K.</creator><creator>Kaw, Meenakshi K.</creator><creator>Lester, Sumona Ghosh</creator><creator>Al-Khudhair, Ahmed</creator><creator>Conran, Philip B.</creator><creator>Chin, Khew-Voon</creator><creator>Gatto-Weis, Cara</creator><creator>Najjar, Sonia M.</creator><general>Elsevier Inc</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200601</creationdate><title>Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice</title><author>Liu, Jehnan ; Muturi, Harrison T. ; Khuder, Saja S. ; Helal, Raghd Abu ; Ghadieh, Hilda E. ; Ramakrishnan, Sadeesh K. ; Kaw, Meenakshi K. ; Lester, Sumona Ghosh ; Al-Khudhair, Ahmed ; Conran, Philip B. ; Chin, Khew-Voon ; Gatto-Weis, Cara ; Najjar, Sonia M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3825-25fca337e9093f5e69edff012d164919d954563e1aa54ba8319cb627deb8aa7a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Carcinoembryonic Antigen - genetics</topic><topic>CEACAM1</topic><topic>Disease Progression</topic><topic>Fatty acid synthase</topic><topic>Haploinsufficiency</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mutation</topic><topic>Neoplasia</topic><topic>Normoinsulinemia</topic><topic>Oncogene Protein v-akt - genetics</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>PML</topic><topic>Prostate intraepithelial neoplasia</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN tumor suppression</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>STAT3 Transcription Factor - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Jehnan</creatorcontrib><creatorcontrib>Muturi, Harrison T.</creatorcontrib><creatorcontrib>Khuder, Saja S.</creatorcontrib><creatorcontrib>Helal, Raghd Abu</creatorcontrib><creatorcontrib>Ghadieh, Hilda E.</creatorcontrib><creatorcontrib>Ramakrishnan, Sadeesh K.</creatorcontrib><creatorcontrib>Kaw, Meenakshi K.</creatorcontrib><creatorcontrib>Lester, Sumona Ghosh</creatorcontrib><creatorcontrib>Al-Khudhair, Ahmed</creatorcontrib><creatorcontrib>Conran, Philip B.</creatorcontrib><creatorcontrib>Chin, Khew-Voon</creatorcontrib><creatorcontrib>Gatto-Weis, Cara</creatorcontrib><creatorcontrib>Najjar, Sonia M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Jehnan</au><au>Muturi, Harrison T.</au><au>Khuder, Saja S.</au><au>Helal, Raghd Abu</au><au>Ghadieh, Hilda E.</au><au>Ramakrishnan, Sadeesh K.</au><au>Kaw, Meenakshi K.</au><au>Lester, Sumona Ghosh</au><au>Al-Khudhair, Ahmed</au><au>Conran, Philip B.</au><au>Chin, Khew-Voon</au><au>Gatto-Weis, Cara</au><au>Najjar, Sonia M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>107</volume><spage>154215</spage><epage>154215</epage><pages>154215-154215</pages><artnum>154215</artnum><issn>0026-0495</issn><issn>1532-8600</issn><eissn>1532-8600</eissn><abstract>PTEN haploinsufficiency plays an important role in prostate cancer development in men. However, monoallelic deletion of Pten gene failed to induce high prostate intraepithelial neoplasia (PIN) until Pten+/− mice aged or fed a high-calorie diet. Because CEACAM1, a cell adhesion molecule with a potential tumor suppression activity, is induced in Pten+/− prostates, the study aimed at examining whether the rise of CEACAM1 limited neoplastic progression in Pten+/− prostates.
Pten+/− were crossbred with Cc1−/− mice harboring a null deletion of Ceacam1 gene to produce Pten+/−/Cc1−/− double mutants. Prostates from 7-month old male mice were analyzed histologically and biochemically for PIN progression.
Deleting Ceacam1 in Pten+/− mice caused an early development of high-grade PIN in parallel to hyperactivation of PI3 kinase/Akt and Ras/MAP kinase pathways, with an increase in cell proliferation, epithelial-to-mesenchymal transition, angiogenesis and inflammation relative to Pten+/− and Cc1−/− individual mutants. It also caused a remarkable increase in lipogenesis in prostate despite maintaining insulin sensitivity. Concomitant Ceacam1 deletion with Pten+/− activated the IL-6/STAT3 signaling pathways to suppress Irf-8 transcription that in turn, led to a decrease in the expression level of promyelocytic leukemia gene, a well characterized tumor suppressor in prostate.
Ceacam1 deletion accelerated high-grade prostate intraepithelial neoplasia in Pten haploinsufficient mice while preserving insulin sensitivity. This demonstrated that the combined loss of Ceacam1 and Pten advanced prostate cancer by increasing lipogenesis and modifying the STAT3-dependent inflammatory microenvironment of prostate.
•CEACAM1-4L expression is elevated in prostates of Pten+/− mice.•Ceacam1 deletion causes progression of neoplasia in prostates of Pten+/− mice.•Ceacam1 deletion causes EMT and angiogenesis in prostates of Pten+/− mice.•Ceacam1 deletion causes lipogenesis and inflammation in prostates of Pten+/− mice.•Ceacam1 deletion activates STAT3 to limit Irf-8 and Pml transcription in Pten+/−.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>32209360</pmid><doi>10.1016/j.metabol.2020.154215</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Carcinoembryonic Antigen - genetics CEACAM1 Disease Progression Fatty acid synthase Haploinsufficiency Male Mice Mice, Inbred C57BL Mice, Knockout Mutation Neoplasia Normoinsulinemia Oncogene Protein v-akt - genetics Phosphatidylinositol 3-Kinases - genetics PML Prostate intraepithelial neoplasia Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology PTEN Phosphohydrolase - genetics PTEN tumor suppression Signal Transduction - drug effects Signal Transduction - genetics STAT3 Transcription Factor - genetics |
| title | Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice |
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