Identification and characterization of transforming growth factor beta‐induced in circulating tumor cell subline from pancreatic cancer cell line
Distant metastasis to liver, lung, brain, or bone occurs by circulating tumor cells (CTC). We hypothesized that a subset of CTC had features that are more malignant than tumor cells at the primary site. We established a highly malignant cell line, Panc‐1‐CTC, derived from the human pancreatic cancer...
Gespeichert in:
Veröffentlicht in: | Cancer science 2018-11, Vol.109 (11), p.3623-3633 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 3633 |
---|---|
container_issue | 11 |
container_start_page | 3623 |
container_title | Cancer science |
container_volume | 109 |
creator | Sato, Taku Muramatsu, Tomoki Tanabe, Minoru Inazawa, Johji |
description | Distant metastasis to liver, lung, brain, or bone occurs by circulating tumor cells (CTC). We hypothesized that a subset of CTC had features that are more malignant than tumor cells at the primary site. We established a highly malignant cell line, Panc‐1‐CTC, derived from the human pancreatic cancer cell line Panc‐1 using an in vivo selection method. Panc‐1‐CTC cells showed greater migratory and invasive abilities than its parent cell line in vitro. In addition, Panc‐1‐CTC cells had a higher tumor‐forming ability than parent cells in vivo. To examine whether a difference in malignant phenotypes exists between Panc‐1‐CTC cells and parent cells, we carried out comprehensive gene expression array analysis. As a result, Panc‐1‐CTC significantly expressed transforming growth factor beta‐induced (TGFBI), an extracellular matrix protein, more abundantly than did parent cells. TGFBI is considered to regulate cell adhesion, but its functions remain unclear. In the present study, knockdown of TGFBI reduced cell migration and invasion abilities, whereas overexpression of TGFBI increased both abilities. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer.
Transforming growth factor beta‐induced (TGFBI) promotes cell migration and invasion abilities in pancreatic cancer. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer. TGFBI could be a novel biomarker for predicting the prognosis of patients with pancreatic cancer. |
doi_str_mv | 10.1111/cas.13783 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6215881</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2289559883</sourcerecordid><originalsourceid>FETCH-LOGICAL-c6173-a77881b51d9810e74ea080b5b3b8a9ca070add35e9d2a04a4d35790e1170b14c3</originalsourceid><addsrcrecordid>eNp1kc9uFSEUxomxsbW68AUMiRtdTAvDMMDGpLnxT5MmLtQ1OQPMvTQzcIUZm3bVRzDxDX0SuZ3bRk1kwxf48XHO-RB6QckJLevUQD6hTEj2CB1R1qhKENI-vtOiUoTVh-hpzpeEsLZRzRN0yAjlLePqCP08ty5MvvcGJh8DhmCx2UACM7nkb5bD2OMpQch9TKMPa7xO8Wra4L5AMeHOTfDr9ocPdjbOYh-w8cnMQ3lb2GkeC2PcMOA8d4MPDvcpjngLwSRXGINNkW7P7IBn6KCHIbvn-_0YfX3_7svqY3Xx6cP56uyiMi0VrAIhpKQdp1ZJSpxoHBBJOt6xToIyQAQBaxl3ytZAGmiKFoo4SgXpaGPYMXq7-G7nbnTWlEEkGPQ2-RHStY7g9d83wW_0On7XbU15-boYvN4bpPhtdnnSo8-7NiC4OGddE9XyMmixQ1_9g17GOYXSnq5rqThXUrJCvVkok2LOyfUPxVCid1HrErW-i7qwL_-s_oG8z7YApwtw5Qd3_X8nvTr7vFj-BgbNt64</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2289559883</pqid></control><display><type>article</type><title>Identification and characterization of transforming growth factor beta‐induced in circulating tumor cell subline from pancreatic cancer cell line</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><creator>Sato, Taku ; Muramatsu, Tomoki ; Tanabe, Minoru ; Inazawa, Johji</creator><creatorcontrib>Sato, Taku ; Muramatsu, Tomoki ; Tanabe, Minoru ; Inazawa, Johji</creatorcontrib><description>Distant metastasis to liver, lung, brain, or bone occurs by circulating tumor cells (CTC). We hypothesized that a subset of CTC had features that are more malignant than tumor cells at the primary site. We established a highly malignant cell line, Panc‐1‐CTC, derived from the human pancreatic cancer cell line Panc‐1 using an in vivo selection method. Panc‐1‐CTC cells showed greater migratory and invasive abilities than its parent cell line in vitro. In addition, Panc‐1‐CTC cells had a higher tumor‐forming ability than parent cells in vivo. To examine whether a difference in malignant phenotypes exists between Panc‐1‐CTC cells and parent cells, we carried out comprehensive gene expression array analysis. As a result, Panc‐1‐CTC significantly expressed transforming growth factor beta‐induced (TGFBI), an extracellular matrix protein, more abundantly than did parent cells. TGFBI is considered to regulate cell adhesion, but its functions remain unclear. In the present study, knockdown of TGFBI reduced cell migration and invasion abilities, whereas overexpression of TGFBI increased both abilities. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer.
Transforming growth factor beta‐induced (TGFBI) promotes cell migration and invasion abilities in pancreatic cancer. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer. TGFBI could be a novel biomarker for predicting the prognosis of patients with pancreatic cancer.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.13783</identifier><identifier>PMID: 30156359</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adhesives ; Animals ; Blood ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - metabolism ; Carcinoma, Pancreatic Ductal - pathology ; Cell adhesion ; Cell adhesion & migration ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; circulating tumor cell (CTC) ; Colorectal cancer ; Cytoplasm ; Extracellular matrix ; extracellular matrix (ECM) ; Extracellular Matrix Proteins - genetics ; Extracellular Matrix Proteins - metabolism ; Gene expression ; Gene Expression Regulation, Neoplastic ; Growth factors ; Humans ; Invasiveness ; in vivo selection ; Matrix protein ; Melanoma ; Metastases ; Metastasis ; Mice ; Neoplasm Transplantation ; Neoplastic Cells, Circulating - metabolism ; Neoplastic Cells, Circulating - pathology ; Original ; Pancreatic cancer ; pancreatic ductal adenocarcinoma (PDAC) ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Phenotypes ; Prognosis ; Proteins ; Survival Analysis ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - metabolism ; transforming growth factor beta‐induced (TGFBI) ; Tumor cells ; Tumors ; Up-Regulation</subject><ispartof>Cancer science, 2018-11, Vol.109 (11), p.3623-3633</ispartof><rights>2018 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2018 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6173-a77881b51d9810e74ea080b5b3b8a9ca070add35e9d2a04a4d35790e1170b14c3</citedby><cites>FETCH-LOGICAL-c6173-a77881b51d9810e74ea080b5b3b8a9ca070add35e9d2a04a4d35790e1170b14c3</cites><orcidid>0000-0002-3945-2800</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6215881/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6215881/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,1412,11543,27905,27906,45555,45556,46033,46457,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30156359$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sato, Taku</creatorcontrib><creatorcontrib>Muramatsu, Tomoki</creatorcontrib><creatorcontrib>Tanabe, Minoru</creatorcontrib><creatorcontrib>Inazawa, Johji</creatorcontrib><title>Identification and characterization of transforming growth factor beta‐induced in circulating tumor cell subline from pancreatic cancer cell line</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Distant metastasis to liver, lung, brain, or bone occurs by circulating tumor cells (CTC). We hypothesized that a subset of CTC had features that are more malignant than tumor cells at the primary site. We established a highly malignant cell line, Panc‐1‐CTC, derived from the human pancreatic cancer cell line Panc‐1 using an in vivo selection method. Panc‐1‐CTC cells showed greater migratory and invasive abilities than its parent cell line in vitro. In addition, Panc‐1‐CTC cells had a higher tumor‐forming ability than parent cells in vivo. To examine whether a difference in malignant phenotypes exists between Panc‐1‐CTC cells and parent cells, we carried out comprehensive gene expression array analysis. As a result, Panc‐1‐CTC significantly expressed transforming growth factor beta‐induced (TGFBI), an extracellular matrix protein, more abundantly than did parent cells. TGFBI is considered to regulate cell adhesion, but its functions remain unclear. In the present study, knockdown of TGFBI reduced cell migration and invasion abilities, whereas overexpression of TGFBI increased both abilities. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer.
Transforming growth factor beta‐induced (TGFBI) promotes cell migration and invasion abilities in pancreatic cancer. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer. TGFBI could be a novel biomarker for predicting the prognosis of patients with pancreatic cancer.</description><subject>Adhesives</subject><subject>Animals</subject><subject>Blood</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>circulating tumor cell (CTC)</subject><subject>Colorectal cancer</subject><subject>Cytoplasm</subject><subject>Extracellular matrix</subject><subject>extracellular matrix (ECM)</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Invasiveness</subject><subject>in vivo selection</subject><subject>Matrix protein</subject><subject>Melanoma</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Neoplasm Transplantation</subject><subject>Neoplastic Cells, Circulating - metabolism</subject><subject>Neoplastic Cells, Circulating - pathology</subject><subject>Original</subject><subject>Pancreatic cancer</subject><subject>pancreatic ductal adenocarcinoma (PDAC)</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Phenotypes</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Survival Analysis</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>transforming growth factor beta‐induced (TGFBI)</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp1kc9uFSEUxomxsbW68AUMiRtdTAvDMMDGpLnxT5MmLtQ1OQPMvTQzcIUZm3bVRzDxDX0SuZ3bRk1kwxf48XHO-RB6QckJLevUQD6hTEj2CB1R1qhKENI-vtOiUoTVh-hpzpeEsLZRzRN0yAjlLePqCP08ty5MvvcGJh8DhmCx2UACM7nkb5bD2OMpQch9TKMPa7xO8Wra4L5AMeHOTfDr9ocPdjbOYh-w8cnMQ3lb2GkeC2PcMOA8d4MPDvcpjngLwSRXGINNkW7P7IBn6KCHIbvn-_0YfX3_7svqY3Xx6cP56uyiMi0VrAIhpKQdp1ZJSpxoHBBJOt6xToIyQAQBaxl3ytZAGmiKFoo4SgXpaGPYMXq7-G7nbnTWlEEkGPQ2-RHStY7g9d83wW_0On7XbU15-boYvN4bpPhtdnnSo8-7NiC4OGddE9XyMmixQ1_9g17GOYXSnq5rqThXUrJCvVkok2LOyfUPxVCid1HrErW-i7qwL_-s_oG8z7YApwtw5Qd3_X8nvTr7vFj-BgbNt64</recordid><startdate>201811</startdate><enddate>201811</enddate><creator>Sato, Taku</creator><creator>Muramatsu, Tomoki</creator><creator>Tanabe, Minoru</creator><creator>Inazawa, Johji</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3945-2800</orcidid></search><sort><creationdate>201811</creationdate><title>Identification and characterization of transforming growth factor beta‐induced in circulating tumor cell subline from pancreatic cancer cell line</title><author>Sato, Taku ; Muramatsu, Tomoki ; Tanabe, Minoru ; Inazawa, Johji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6173-a77881b51d9810e74ea080b5b3b8a9ca070add35e9d2a04a4d35790e1170b14c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adhesives</topic><topic>Animals</topic><topic>Blood</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - metabolism</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>circulating tumor cell (CTC)</topic><topic>Colorectal cancer</topic><topic>Cytoplasm</topic><topic>Extracellular matrix</topic><topic>extracellular matrix (ECM)</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Invasiveness</topic><topic>in vivo selection</topic><topic>Matrix protein</topic><topic>Melanoma</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Neoplasm Transplantation</topic><topic>Neoplastic Cells, Circulating - metabolism</topic><topic>Neoplastic Cells, Circulating - pathology</topic><topic>Original</topic><topic>Pancreatic cancer</topic><topic>pancreatic ductal adenocarcinoma (PDAC)</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Phenotypes</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Survival Analysis</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>transforming growth factor beta‐induced (TGFBI)</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sato, Taku</creatorcontrib><creatorcontrib>Muramatsu, Tomoki</creatorcontrib><creatorcontrib>Tanabe, Minoru</creatorcontrib><creatorcontrib>Inazawa, Johji</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sato, Taku</au><au>Muramatsu, Tomoki</au><au>Tanabe, Minoru</au><au>Inazawa, Johji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification and characterization of transforming growth factor beta‐induced in circulating tumor cell subline from pancreatic cancer cell line</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2018-11</date><risdate>2018</risdate><volume>109</volume><issue>11</issue><spage>3623</spage><epage>3633</epage><pages>3623-3633</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Distant metastasis to liver, lung, brain, or bone occurs by circulating tumor cells (CTC). We hypothesized that a subset of CTC had features that are more malignant than tumor cells at the primary site. We established a highly malignant cell line, Panc‐1‐CTC, derived from the human pancreatic cancer cell line Panc‐1 using an in vivo selection method. Panc‐1‐CTC cells showed greater migratory and invasive abilities than its parent cell line in vitro. In addition, Panc‐1‐CTC cells had a higher tumor‐forming ability than parent cells in vivo. To examine whether a difference in malignant phenotypes exists between Panc‐1‐CTC cells and parent cells, we carried out comprehensive gene expression array analysis. As a result, Panc‐1‐CTC significantly expressed transforming growth factor beta‐induced (TGFBI), an extracellular matrix protein, more abundantly than did parent cells. TGFBI is considered to regulate cell adhesion, but its functions remain unclear. In the present study, knockdown of TGFBI reduced cell migration and invasion abilities, whereas overexpression of TGFBI increased both abilities. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer.
Transforming growth factor beta‐induced (TGFBI) promotes cell migration and invasion abilities in pancreatic cancer. Moreover, elevated expression of TGFBI was associated with poor prognosis in patients with pancreatic cancer. TGFBI could be a novel biomarker for predicting the prognosis of patients with pancreatic cancer.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>30156359</pmid><doi>10.1111/cas.13783</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-3945-2800</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1347-9032 |
ispartof | Cancer science, 2018-11, Vol.109 (11), p.3623-3633 |
issn | 1347-9032 1349-7006 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6215881 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Wiley-Blackwell Open Access Titles; PubMed Central |
subjects | Adhesives Animals Blood Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - pathology Cell adhesion Cell adhesion & migration Cell growth Cell Line, Tumor Cell migration Cell Movement Cell Proliferation circulating tumor cell (CTC) Colorectal cancer Cytoplasm Extracellular matrix extracellular matrix (ECM) Extracellular Matrix Proteins - genetics Extracellular Matrix Proteins - metabolism Gene expression Gene Expression Regulation, Neoplastic Growth factors Humans Invasiveness in vivo selection Matrix protein Melanoma Metastases Metastasis Mice Neoplasm Transplantation Neoplastic Cells, Circulating - metabolism Neoplastic Cells, Circulating - pathology Original Pancreatic cancer pancreatic ductal adenocarcinoma (PDAC) Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Phenotypes Prognosis Proteins Survival Analysis Transforming Growth Factor beta - genetics Transforming Growth Factor beta - metabolism transforming growth factor beta‐induced (TGFBI) Tumor cells Tumors Up-Regulation |
title | Identification and characterization of transforming growth factor beta‐induced in circulating tumor cell subline from pancreatic cancer cell line |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T20%3A04%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Identification%20and%20characterization%20of%20transforming%20growth%20factor%20beta%E2%80%90induced%20in%20circulating%20tumor%20cell%20subline%20from%20pancreatic%20cancer%20cell%20line&rft.jtitle=Cancer%20science&rft.au=Sato,%20Taku&rft.date=2018-11&rft.volume=109&rft.issue=11&rft.spage=3623&rft.epage=3633&rft.pages=3623-3633&rft.issn=1347-9032&rft.eissn=1349-7006&rft_id=info:doi/10.1111/cas.13783&rft_dat=%3Cproquest_pubme%3E2289559883%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2289559883&rft_id=info:pmid/30156359&rfr_iscdi=true |