Involvement of CXCL14 in osteolytic bone metastasis from lung cancer
To investigate the molecular mechanisms of lung cancer-induced bone metastasis, we established a bone-seeking subclone (HARA-B4) from a human squamous lung cancer cell line (HARA) using an in vivo selection method. We compared comprehensive gene expression profiles between HARA and HARA-B4, and iden...
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| Veröffentlicht in: | International journal of oncology 2014-04, Vol.44 (4), p.1316-1324 |
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| creator | TAKIGUCHI, SOICHI KORENAGA, NATSUKI INOUE, KAZUKO SUGI, ERIKA KATAOKA, YASUFUMI MATSUSUE, KIMIHIKO FUTAGAMI, KOUJIRO LI, YIN-JI KUKITA, TOSHIO TERAMOTO, NORIHIRO IGUCHI, HARUO |
| description | To investigate the molecular mechanisms of lung cancer-induced bone metastasis, we established a bone-seeking subclone (HARA-B4) from a human squamous lung cancer cell line (HARA) using an in vivo selection method. We compared comprehensive gene expression profiles between HARA and HARA-B4, and identified the critical factors for the formation of bone metastasis using in vitro and in vivo assays. The number of bone metastatic colonies in the hind legs was significantly higher in HARA-B4-inoculated mice than in HARA-inoculated mice at 4 weeks after inoculation. In addition, visceral (adrenal) metastases were not found in HARA-B4-inoculated mice at autopsy, suggesting an increase in cancer cell tropism to bone in HARA-B4. Based on a comprehensive gene expression analysis, the expression level of CXC chemokine ligand 14 (CXCL14) was 5-fold greater in HARA-B4 than in HARA. Results of a soft agar colony formation assay showed that anchorage-independent growth ability was 4.5-fold higher with HARA-B4 than with HARA. The murine pre-osteoblast cell line MC3T3-E1 and the preosteoclast/macrophage cell line RAW264.7 migrated faster toward cultured HARA-B4 cells than toward HARA cells in a transwell cell migration assay. Interestingly, CXCL14 was shown to be involved in all events (enhancement of cancer cell tropism to the bone, anchorage-independent growth and/or recruitment of bone marrow cells) based on siRNA experiments in HARA-B4 cells. Furthermore, in clinical specimens of lung cancer-induced bone metastasis, expression of CXCL14 was observed in the tumor cells infiltrated in bone marrow in all specimens examined. CXCL14 was able to promote bone metastasis through enhancement of cancer cell tropism to the bone and/or recruitment of bone marrow cells around meta-static cancer cells. |
| doi_str_mv | 10.3892/ijo.2014.2293 |
| format | Article |
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We compared comprehensive gene expression profiles between HARA and HARA-B4, and identified the critical factors for the formation of bone metastasis using in vitro and in vivo assays. The number of bone metastatic colonies in the hind legs was significantly higher in HARA-B4-inoculated mice than in HARA-inoculated mice at 4 weeks after inoculation. In addition, visceral (adrenal) metastases were not found in HARA-B4-inoculated mice at autopsy, suggesting an increase in cancer cell tropism to bone in HARA-B4. Based on a comprehensive gene expression analysis, the expression level of CXC chemokine ligand 14 (CXCL14) was 5-fold greater in HARA-B4 than in HARA. Results of a soft agar colony formation assay showed that anchorage-independent growth ability was 4.5-fold higher with HARA-B4 than with HARA. The murine pre-osteoblast cell line MC3T3-E1 and the preosteoclast/macrophage cell line RAW264.7 migrated faster toward cultured HARA-B4 cells than toward HARA cells in a transwell cell migration assay. Interestingly, CXCL14 was shown to be involved in all events (enhancement of cancer cell tropism to the bone, anchorage-independent growth and/or recruitment of bone marrow cells) based on siRNA experiments in HARA-B4 cells. Furthermore, in clinical specimens of lung cancer-induced bone metastasis, expression of CXCL14 was observed in the tumor cells infiltrated in bone marrow in all specimens examined. CXCL14 was able to promote bone metastasis through enhancement of cancer cell tropism to the bone and/or recruitment of bone marrow cells around meta-static cancer cells.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2014.2293</identifier><identifier>PMID: 24534874</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adrenal glands ; anchorage-independent growth ; Animals ; Bone cancer ; Bone marrow ; bone metastasis ; Bone Neoplasms - pathology ; Bone Neoplasms - secondary ; Cell growth ; Cell Line, Tumor ; Cell Movement ; Chemokines ; Chemokines, CXC - biosynthesis ; Chemokines, CXC - genetics ; chemotaxis ; Complications and side effects ; CXCL14 ; Cytokines ; Development and progression ; Gene expression ; Health aspects ; Humans ; Ligands ; Lung cancer ; Lung Neoplasms - etiology ; Lung Neoplasms - pathology ; Macrophages - metabolism ; Male ; Metastasis ; Mice ; Osteoblasts - metabolism ; Osteoblasts - pathology ; Osteoclasts - pathology ; Osteolysis - complications ; Osteolysis - pathology ; Penicillin ; Population ; Rats ; Rats, Sprague-Dawley ; Risk factors ; RNA Interference ; RNA, Small Interfering</subject><ispartof>International journal of oncology, 2014-04, Vol.44 (4), p.1316-1324</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-583b0fb9429e6b040f1acbb22a3deaceb687887327bff6526c5d6bd93b8a00853</citedby><cites>FETCH-LOGICAL-c451t-583b0fb9429e6b040f1acbb22a3deaceb687887327bff6526c5d6bd93b8a00853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24534874$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TAKIGUCHI, SOICHI</creatorcontrib><creatorcontrib>KORENAGA, NATSUKI</creatorcontrib><creatorcontrib>INOUE, KAZUKO</creatorcontrib><creatorcontrib>SUGI, ERIKA</creatorcontrib><creatorcontrib>KATAOKA, YASUFUMI</creatorcontrib><creatorcontrib>MATSUSUE, KIMIHIKO</creatorcontrib><creatorcontrib>FUTAGAMI, KOUJIRO</creatorcontrib><creatorcontrib>LI, YIN-JI</creatorcontrib><creatorcontrib>KUKITA, TOSHIO</creatorcontrib><creatorcontrib>TERAMOTO, NORIHIRO</creatorcontrib><creatorcontrib>IGUCHI, HARUO</creatorcontrib><title>Involvement of CXCL14 in osteolytic bone metastasis from lung cancer</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>To investigate the molecular mechanisms of lung cancer-induced bone metastasis, we established a bone-seeking subclone (HARA-B4) from a human squamous lung cancer cell line (HARA) using an in vivo selection method. We compared comprehensive gene expression profiles between HARA and HARA-B4, and identified the critical factors for the formation of bone metastasis using in vitro and in vivo assays. The number of bone metastatic colonies in the hind legs was significantly higher in HARA-B4-inoculated mice than in HARA-inoculated mice at 4 weeks after inoculation. In addition, visceral (adrenal) metastases were not found in HARA-B4-inoculated mice at autopsy, suggesting an increase in cancer cell tropism to bone in HARA-B4. Based on a comprehensive gene expression analysis, the expression level of CXC chemokine ligand 14 (CXCL14) was 5-fold greater in HARA-B4 than in HARA. Results of a soft agar colony formation assay showed that anchorage-independent growth ability was 4.5-fold higher with HARA-B4 than with HARA. The murine pre-osteoblast cell line MC3T3-E1 and the preosteoclast/macrophage cell line RAW264.7 migrated faster toward cultured HARA-B4 cells than toward HARA cells in a transwell cell migration assay. Interestingly, CXCL14 was shown to be involved in all events (enhancement of cancer cell tropism to the bone, anchorage-independent growth and/or recruitment of bone marrow cells) based on siRNA experiments in HARA-B4 cells. Furthermore, in clinical specimens of lung cancer-induced bone metastasis, expression of CXCL14 was observed in the tumor cells infiltrated in bone marrow in all specimens examined. CXCL14 was able to promote bone metastasis through enhancement of cancer cell tropism to the bone and/or recruitment of bone marrow cells around meta-static cancer cells.</description><subject>Adrenal glands</subject><subject>anchorage-independent growth</subject><subject>Animals</subject><subject>Bone cancer</subject><subject>Bone marrow</subject><subject>bone metastasis</subject><subject>Bone Neoplasms - pathology</subject><subject>Bone Neoplasms - secondary</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Chemokines</subject><subject>Chemokines, CXC - biosynthesis</subject><subject>Chemokines, CXC - genetics</subject><subject>chemotaxis</subject><subject>Complications and side effects</subject><subject>CXCL14</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Ligands</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - etiology</subject><subject>Lung Neoplasms - pathology</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Osteoblasts - metabolism</subject><subject>Osteoblasts - pathology</subject><subject>Osteoclasts - pathology</subject><subject>Osteolysis - complications</subject><subject>Osteolysis - pathology</subject><subject>Penicillin</subject><subject>Population</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Risk factors</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpV0ctrHCEcB3AJLXm1x1yLUGhObn2NMx7Dtk0CC7200Juoo4nLjG7VCeS_j8umSQqCHj78Hn4BuCB4xQZJv4ZtWlFM-IpSyY7AKeklQZRT9q69MZFIcCZPwFkpW4xp12FyDE4o7xgfen4Kvt3GhzQ9uNnFCpOH6z_rDeEwRJhKdWl6rMFCk6KDs6u6tBMK9DnNcFriHbQ6Wpc_gPdeT8V9fL7Pwe8f33-tb9Dm5_Xt-mqDLO9IRd3ADPZGciqdMJhjT7Q1hlLNRqetM2Loh6FntDfei44K243CjJKZQWM8dOwcfD7U3eX0d3Glqm1acmwtFZGMMkrbgq_qTk9OhehTzdrOoVh1xUkTQjDc1Jc36t7pqd6XNC01pFj-h-gAbU6lZOfVLodZ50dFsNpHoFoEah-B2kfQ_KfnIRczu_FF__vzBi4PoOx0HMOYyotplRDnCHNEGBHsCdSai5k</recordid><startdate>20140401</startdate><enddate>20140401</enddate><creator>TAKIGUCHI, SOICHI</creator><creator>KORENAGA, NATSUKI</creator><creator>INOUE, KAZUKO</creator><creator>SUGI, ERIKA</creator><creator>KATAOKA, YASUFUMI</creator><creator>MATSUSUE, KIMIHIKO</creator><creator>FUTAGAMI, KOUJIRO</creator><creator>LI, YIN-JI</creator><creator>KUKITA, TOSHIO</creator><creator>TERAMOTO, NORIHIRO</creator><creator>IGUCHI, HARUO</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20140401</creationdate><title>Involvement of CXCL14 in osteolytic bone metastasis from lung cancer</title><author>TAKIGUCHI, SOICHI ; KORENAGA, NATSUKI ; INOUE, KAZUKO ; SUGI, ERIKA ; KATAOKA, YASUFUMI ; MATSUSUE, KIMIHIKO ; FUTAGAMI, KOUJIRO ; LI, YIN-JI ; KUKITA, TOSHIO ; TERAMOTO, NORIHIRO ; IGUCHI, HARUO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-583b0fb9429e6b040f1acbb22a3deaceb687887327bff6526c5d6bd93b8a00853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adrenal glands</topic><topic>anchorage-independent growth</topic><topic>Animals</topic><topic>Bone cancer</topic><topic>Bone marrow</topic><topic>bone metastasis</topic><topic>Bone Neoplasms - pathology</topic><topic>Bone Neoplasms - secondary</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Chemokines</topic><topic>Chemokines, CXC - biosynthesis</topic><topic>Chemokines, CXC - genetics</topic><topic>chemotaxis</topic><topic>Complications and side effects</topic><topic>CXCL14</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Ligands</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - etiology</topic><topic>Lung Neoplasms - pathology</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Osteoblasts - metabolism</topic><topic>Osteoblasts - pathology</topic><topic>Osteoclasts - pathology</topic><topic>Osteolysis - complications</topic><topic>Osteolysis - pathology</topic><topic>Penicillin</topic><topic>Population</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Risk factors</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TAKIGUCHI, SOICHI</creatorcontrib><creatorcontrib>KORENAGA, NATSUKI</creatorcontrib><creatorcontrib>INOUE, KAZUKO</creatorcontrib><creatorcontrib>SUGI, ERIKA</creatorcontrib><creatorcontrib>KATAOKA, YASUFUMI</creatorcontrib><creatorcontrib>MATSUSUE, KIMIHIKO</creatorcontrib><creatorcontrib>FUTAGAMI, KOUJIRO</creatorcontrib><creatorcontrib>LI, YIN-JI</creatorcontrib><creatorcontrib>KUKITA, TOSHIO</creatorcontrib><creatorcontrib>TERAMOTO, NORIHIRO</creatorcontrib><creatorcontrib>IGUCHI, HARUO</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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 China</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>TAKIGUCHI, SOICHI</au><au>KORENAGA, NATSUKI</au><au>INOUE, KAZUKO</au><au>SUGI, ERIKA</au><au>KATAOKA, YASUFUMI</au><au>MATSUSUE, KIMIHIKO</au><au>FUTAGAMI, KOUJIRO</au><au>LI, YIN-JI</au><au>KUKITA, TOSHIO</au><au>TERAMOTO, NORIHIRO</au><au>IGUCHI, HARUO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of CXCL14 in osteolytic bone metastasis from lung cancer</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2014-04-01</date><risdate>2014</risdate><volume>44</volume><issue>4</issue><spage>1316</spage><epage>1324</epage><pages>1316-1324</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>To investigate the molecular mechanisms of lung cancer-induced bone metastasis, we established a bone-seeking subclone (HARA-B4) from a human squamous lung cancer cell line (HARA) using an in vivo selection method. We compared comprehensive gene expression profiles between HARA and HARA-B4, and identified the critical factors for the formation of bone metastasis using in vitro and in vivo assays. The number of bone metastatic colonies in the hind legs was significantly higher in HARA-B4-inoculated mice than in HARA-inoculated mice at 4 weeks after inoculation. In addition, visceral (adrenal) metastases were not found in HARA-B4-inoculated mice at autopsy, suggesting an increase in cancer cell tropism to bone in HARA-B4. Based on a comprehensive gene expression analysis, the expression level of CXC chemokine ligand 14 (CXCL14) was 5-fold greater in HARA-B4 than in HARA. Results of a soft agar colony formation assay showed that anchorage-independent growth ability was 4.5-fold higher with HARA-B4 than with HARA. The murine pre-osteoblast cell line MC3T3-E1 and the preosteoclast/macrophage cell line RAW264.7 migrated faster toward cultured HARA-B4 cells than toward HARA cells in a transwell cell migration assay. Interestingly, CXCL14 was shown to be involved in all events (enhancement of cancer cell tropism to the bone, anchorage-independent growth and/or recruitment of bone marrow cells) based on siRNA experiments in HARA-B4 cells. Furthermore, in clinical specimens of lung cancer-induced bone metastasis, expression of CXCL14 was observed in the tumor cells infiltrated in bone marrow in all specimens examined. CXCL14 was able to promote bone metastasis through enhancement of cancer cell tropism to the bone and/or recruitment of bone marrow cells around meta-static cancer cells.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24534874</pmid><doi>10.3892/ijo.2014.2293</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of oncology, 2014-04, Vol.44 (4), p.1316-1324 |
| issn | 1019-6439 1791-2423 |
| language | eng |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adrenal glands anchorage-independent growth Animals Bone cancer Bone marrow bone metastasis Bone Neoplasms - pathology Bone Neoplasms - secondary Cell growth Cell Line, Tumor Cell Movement Chemokines Chemokines, CXC - biosynthesis Chemokines, CXC - genetics chemotaxis Complications and side effects CXCL14 Cytokines Development and progression Gene expression Health aspects Humans Ligands Lung cancer Lung Neoplasms - etiology Lung Neoplasms - pathology Macrophages - metabolism Male Metastasis Mice Osteoblasts - metabolism Osteoblasts - pathology Osteoclasts - pathology Osteolysis - complications Osteolysis - pathology Penicillin Population Rats Rats, Sprague-Dawley Risk factors RNA Interference RNA, Small Interfering |
| title | Involvement of CXCL14 in osteolytic bone metastasis from lung cancer |
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