Somatostatin Derivate
Tumor development and progression are influenced by macrophages of the surrounding microenvironment. To investigate the influences of an inflammatory tumor microenvironment on the growth and metastasis of prostate cancer, the present study used a co-culture model of prostate cancer (PCa) cells with...
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| Veröffentlicht in: | PloS one 2015-05, Vol.10 (5) |
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| container_title | PloS one |
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| creator | Guo, Zhaoxin Xing, Zhaoquan Cheng, Xiangyu Fang, Zhiqing Jiang, Chao Su, Jing Zhou, Zunlin Xu, Zhonghua Holmberg, Anders Nilsson, Sten Liu, Zhaoxu |
| description | Tumor development and progression are influenced by macrophages of the surrounding microenvironment. To investigate the influences of an inflammatory tumor microenvironment on the growth and metastasis of prostate cancer, the present study used a co-culture model of prostate cancer (PCa) cells with tumor-associated macrophage (TAM)-conditioned medium (MCM). MCM promoted PCa cell (LNCaP, DU145 and PC-3) growth, and a xenograft model in nude mice consistently demonstrated that MCM could promote tumor growth. MCM also stimulated migration and invasion in vitro. Somatostatin derivate (smsDX) significantly attenuated the TAM-stimulated proliferation, migration and invasion of prostate cancer. Immunohistochemistry revealed that NF-[kappa]B was over-expressed in PCa and BPH with chronic inflammatory tissue specimens and was positively correlated with macrophage infiltration. Further investigation into the underlying mechanism revealed that NF-[kappa]B played an important role in macrophage infiltration. SmsDX inhibited the paracrine loop between TAM and PCa cells and may represent a potential therapeutic agent for PCa. |
| doi_str_mv | 10.1371/journal.pone.0124292 |
| format | Article |
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To investigate the influences of an inflammatory tumor microenvironment on the growth and metastasis of prostate cancer, the present study used a co-culture model of prostate cancer (PCa) cells with tumor-associated macrophage (TAM)-conditioned medium (MCM). MCM promoted PCa cell (LNCaP, DU145 and PC-3) growth, and a xenograft model in nude mice consistently demonstrated that MCM could promote tumor growth. MCM also stimulated migration and invasion in vitro. Somatostatin derivate (smsDX) significantly attenuated the TAM-stimulated proliferation, migration and invasion of prostate cancer. Immunohistochemistry revealed that NF-[kappa]B was over-expressed in PCa and BPH with chronic inflammatory tissue specimens and was positively correlated with macrophage infiltration. Further investigation into the underlying mechanism revealed that NF-[kappa]B played an important role in macrophage infiltration. 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To investigate the influences of an inflammatory tumor microenvironment on the growth and metastasis of prostate cancer, the present study used a co-culture model of prostate cancer (PCa) cells with tumor-associated macrophage (TAM)-conditioned medium (MCM). MCM promoted PCa cell (LNCaP, DU145 and PC-3) growth, and a xenograft model in nude mice consistently demonstrated that MCM could promote tumor growth. MCM also stimulated migration and invasion in vitro. Somatostatin derivate (smsDX) significantly attenuated the TAM-stimulated proliferation, migration and invasion of prostate cancer. Immunohistochemistry revealed that NF-[kappa]B was over-expressed in PCa and BPH with chronic inflammatory tissue specimens and was positively correlated with macrophage infiltration. Further investigation into the underlying mechanism revealed that NF-[kappa]B played an important role in macrophage infiltration. SmsDX inhibited the paracrine loop between TAM and PCa cells and may represent a potential therapeutic agent for PCa.</description><subject>Analysis</subject><subject>Cancer cells</subject><subject>Development and progression</subject><subject>Physiological aspects</subject><subject>Prostate cancer</subject><subject>Somatostatin</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNqFzD1PwzAUhWELgUQpjGwMTEgMCb52nPqOVfmqVKkSrVijm3Cdpgo2qh3Ez2eAIUxM5x0eHSGuQOagZ3C3D8PBU59_BM-5BFUoVEdiAqhVViqpj0d9Ks5i3EtptC3LibjchHdKISZKnb--50P3SYnPxYmjPvLF707F9vFhu3jOVuun5WK-ylpEm7FBALRmhlxodoUFkAoNldjUzkFBzljNqElJA2-1RWW4aZCdq4lQWz0Vtz-3LfVcdb4JPvFXammIsVpuXqp5oZWB0sB_dv36196M7I6pT7sY-iF1wccx_AYKAVqg</recordid><startdate>20150526</startdate><enddate>20150526</enddate><creator>Guo, Zhaoxin</creator><creator>Xing, Zhaoquan</creator><creator>Cheng, Xiangyu</creator><creator>Fang, Zhiqing</creator><creator>Jiang, Chao</creator><creator>Su, Jing</creator><creator>Zhou, Zunlin</creator><creator>Xu, Zhonghua</creator><creator>Holmberg, Anders</creator><creator>Nilsson, Sten</creator><creator>Liu, Zhaoxu</creator><general>Public Library of Science</general><scope>IOV</scope><scope>ISR</scope></search><sort><creationdate>20150526</creationdate><title>Somatostatin Derivate</title><author>Guo, Zhaoxin ; Xing, Zhaoquan ; Cheng, Xiangyu ; Fang, Zhiqing ; Jiang, Chao ; Su, Jing ; Zhou, Zunlin ; Xu, Zhonghua ; Holmberg, Anders ; Nilsson, Sten ; Liu, Zhaoxu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g998-e591198579e43ef48110295a69cbff14af583e93a2051db8925ecc9effbaa9383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Cancer cells</topic><topic>Development and progression</topic><topic>Physiological aspects</topic><topic>Prostate cancer</topic><topic>Somatostatin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Zhaoxin</creatorcontrib><creatorcontrib>Xing, Zhaoquan</creatorcontrib><creatorcontrib>Cheng, Xiangyu</creatorcontrib><creatorcontrib>Fang, Zhiqing</creatorcontrib><creatorcontrib>Jiang, Chao</creatorcontrib><creatorcontrib>Su, Jing</creatorcontrib><creatorcontrib>Zhou, Zunlin</creatorcontrib><creatorcontrib>Xu, Zhonghua</creatorcontrib><creatorcontrib>Holmberg, Anders</creatorcontrib><creatorcontrib>Nilsson, Sten</creatorcontrib><creatorcontrib>Liu, Zhaoxu</creatorcontrib><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Zhaoxin</au><au>Xing, Zhaoquan</au><au>Cheng, Xiangyu</au><au>Fang, Zhiqing</au><au>Jiang, Chao</au><au>Su, Jing</au><au>Zhou, Zunlin</au><au>Xu, Zhonghua</au><au>Holmberg, Anders</au><au>Nilsson, Sten</au><au>Liu, Zhaoxu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Somatostatin Derivate</atitle><jtitle>PloS one</jtitle><date>2015-05-26</date><risdate>2015</risdate><volume>10</volume><issue>5</issue><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Tumor development and progression are influenced by macrophages of the surrounding microenvironment. To investigate the influences of an inflammatory tumor microenvironment on the growth and metastasis of prostate cancer, the present study used a co-culture model of prostate cancer (PCa) cells with tumor-associated macrophage (TAM)-conditioned medium (MCM). MCM promoted PCa cell (LNCaP, DU145 and PC-3) growth, and a xenograft model in nude mice consistently demonstrated that MCM could promote tumor growth. MCM also stimulated migration and invasion in vitro. Somatostatin derivate (smsDX) significantly attenuated the TAM-stimulated proliferation, migration and invasion of prostate cancer. Immunohistochemistry revealed that NF-[kappa]B was over-expressed in PCa and BPH with chronic inflammatory tissue specimens and was positively correlated with macrophage infiltration. Further investigation into the underlying mechanism revealed that NF-[kappa]B played an important role in macrophage infiltration. 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| subjects | Analysis Cancer cells Development and progression Physiological aspects Prostate cancer Somatostatin |
| title | Somatostatin Derivate |
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