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...

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Veröffentlicht in:Cancer science 2018-11, Vol.109 (11), p.3623-3633
Hauptverfasser: Sato, Taku, Muramatsu, Tomoki, Tanabe, Minoru, Inazawa, Johji
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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.
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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. 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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. 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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 &amp; 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>
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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
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