Tumor cells enhance their own CD44 cleavage and motility by generating hyaluronan fragments.
Identifieur interne : 002C84 ( Main/Exploration ); précédent : 002C83; suivant : 002C85Tumor cells enhance their own CD44 cleavage and motility by generating hyaluronan fragments.
Auteurs : Kazuki N. Sugahara [Japon] ; Takako Hirata ; Haruko Hayasaka ; Robert Stern ; Toshiyuki Murai ; Masayuki MiyasakaSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 2006.
Descripteurs français
- KwdFr :
- Acide hyaluronique (), Acide hyaluronique (métabolisme), Animaux, Communication autocrine, Communication paracrine, Humains, Hyaluronoglucosaminidase (métabolisme), Lignée cellulaire tumorale, Masse moléculaire, Mouvement cellulaire, Oligosaccharides (), Oligosaccharides (métabolisme), Tumeurs (anatomopathologie), Tumeurs (métabolisme).
- MESH :
- anatomopathologie : Tumeurs.
- métabolisme : Acide hyaluronique, Hyaluronoglucosaminidase, Oligosaccharides, Tumeurs.
- Acide hyaluronique, Animaux, Communication autocrine, Communication paracrine, Humains, Lignée cellulaire tumorale, Masse moléculaire, Mouvement cellulaire, Oligosaccharides.
English descriptors
- KwdEn :
- Animals, Autocrine Communication, Cell Line, Tumor, Cell Movement, Humans, Hyaluronan Receptors (metabolism), Hyaluronic Acid (chemistry), Hyaluronic Acid (metabolism), Hyaluronoglucosaminidase (metabolism), Molecular Weight, Neoplasms (metabolism), Neoplasms (pathology), Oligosaccharides (chemistry), Oligosaccharides (metabolism), Paracrine Communication.
- MESH :
- chemical , chemistry : Hyaluronic Acid, Oligosaccharides.
- chemical , metabolism : Hyaluronan Receptors, Hyaluronic Acid, Hyaluronoglucosaminidase, Oligosaccharides.
- metabolism : Neoplasms.
- pathology : Neoplasms.
- Animals, Autocrine Communication, Cell Line, Tumor, Cell Movement, Humans, Molecular Weight, Paracrine Communication.
Abstract
Hyaluronan (HA) is an extracellular matrix glycosaminoglycan that interacts with cell-surface receptors, including CD44. Although HA usually exists as a high molecular mass polymer, HA of a much lower molecular mass that shows a variety of biological activities can be detected under certain pathological conditions, particularly in tumors. We previously reported that low molecular weight HAs (LMW-HAs) of a certain size range induce the proteolytic cleavage of CD44 from the surface of tumor cells and promote tumor cell migration in a CD44-dependent manner. Here, we show that MIA PaCa-2, a human pancreatic carcinoma cell line, secreted hyaluronidases abundantly and generated readily detectable levels of LMW-HAs ranging from approximately 10- to 40-mers. This occurred in the absence of any exogenous stimulation. The tumor-derived HA oligosaccharides were able to enhance CD44 cleavage and tumor cell motility. Inhibition of the CD44-HA interaction resulted in the complete abrogation of these cellular events. These results are consistent with the concept that tumor cells generate HA oligosaccha-rides that bind to tumor cell CD44 through the expression of their own constitutive hyaluronidases. This enhances their own CD44 cleavage and cell motility, which would subsequently promote tumor progression. Such an autocrine/paracrine-like process may represent a novel activation mechanism that would facilitate and promote the malignant potential of tumor cells.
DOI: 10.1074/jbc.M506740200
PubMed: 16407205
Affiliations:
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Le document en format XML
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Sugahara</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Immunodynamics, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Immunodynamics, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871</wicri:regionArea><wicri:noRegion>Osaka 565-0871</wicri:noRegion></affiliation></author><author><name sortKey="Hirata, Takako" sort="Hirata, Takako" uniqKey="Hirata T" first="Takako" last="Hirata">Takako Hirata</name></author><author><name sortKey="Hayasaka, Haruko" sort="Hayasaka, Haruko" uniqKey="Hayasaka H" first="Haruko" last="Hayasaka">Haruko Hayasaka</name></author><author><name sortKey="Stern, Robert" sort="Stern, Robert" uniqKey="Stern R" first="Robert" last="Stern">Robert Stern</name></author><author><name sortKey="Murai, Toshiyuki" sort="Murai, Toshiyuki" uniqKey="Murai T" first="Toshiyuki" last="Murai">Toshiyuki Murai</name></author><author><name sortKey="Miyasaka, Masayuki" sort="Miyasaka, Masayuki" uniqKey="Miyasaka M" first="Masayuki" last="Miyasaka">Masayuki Miyasaka</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="ISSN">0021-9258</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autocrine Communication</term><term>Cell Line, Tumor</term><term>Cell Movement</term><term>Humans</term><term>Hyaluronan Receptors (metabolism)</term><term>Hyaluronic Acid (chemistry)</term><term>Hyaluronic Acid (metabolism)</term><term>Hyaluronoglucosaminidase (metabolism)</term><term>Molecular Weight</term><term>Neoplasms (metabolism)</term><term>Neoplasms (pathology)</term><term>Oligosaccharides (chemistry)</term><term>Oligosaccharides (metabolism)</term><term>Paracrine Communication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide hyaluronique ()</term><term>Acide hyaluronique (métabolisme)</term><term>Animaux</term><term>Communication autocrine</term><term>Communication paracrine</term><term>Humains</term><term>Hyaluronoglucosaminidase (métabolisme)</term><term>Lignée cellulaire tumorale</term><term>Masse moléculaire</term><term>Mouvement cellulaire</term><term>Oligosaccharides ()</term><term>Oligosaccharides (métabolisme)</term><term>Tumeurs (anatomopathologie)</term><term>Tumeurs (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Hyaluronic Acid</term><term>Oligosaccharides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hyaluronan Receptors</term><term>Hyaluronic Acid</term><term>Hyaluronoglucosaminidase</term><term>Oligosaccharides</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acide hyaluronique</term><term>Hyaluronoglucosaminidase</term><term>Oligosaccharides</term><term>Tumeurs</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autocrine Communication</term><term>Cell Line, Tumor</term><term>Cell Movement</term><term>Humans</term><term>Molecular Weight</term><term>Paracrine Communication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Acide hyaluronique</term><term>Animaux</term><term>Communication autocrine</term><term>Communication paracrine</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Masse moléculaire</term><term>Mouvement cellulaire</term><term>Oligosaccharides</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hyaluronan (HA) is an extracellular matrix glycosaminoglycan that interacts with cell-surface receptors, including CD44. Although HA usually exists as a high molecular mass polymer, HA of a much lower molecular mass that shows a variety of biological activities can be detected under certain pathological conditions, particularly in tumors. We previously reported that low molecular weight HAs (LMW-HAs) of a certain size range induce the proteolytic cleavage of CD44 from the surface of tumor cells and promote tumor cell migration in a CD44-dependent manner. Here, we show that MIA PaCa-2, a human pancreatic carcinoma cell line, secreted hyaluronidases abundantly and generated readily detectable levels of LMW-HAs ranging from approximately 10- to 40-mers. This occurred in the absence of any exogenous stimulation. The tumor-derived HA oligosaccharides were able to enhance CD44 cleavage and tumor cell motility. Inhibition of the CD44-HA interaction resulted in the complete abrogation of these cellular events. These results are consistent with the concept that tumor cells generate HA oligosaccha-rides that bind to tumor cell CD44 through the expression of their own constitutive hyaluronidases. This enhances their own CD44 cleavage and cell motility, which would subsequently promote tumor progression. Such an autocrine/paracrine-like process may represent a novel activation mechanism that would facilitate and promote the malignant potential of tumor cells.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Hayasaka, Haruko" sort="Hayasaka, Haruko" uniqKey="Hayasaka H" first="Haruko" last="Hayasaka">Haruko Hayasaka</name><name sortKey="Hirata, Takako" sort="Hirata, Takako" uniqKey="Hirata T" first="Takako" last="Hirata">Takako Hirata</name><name sortKey="Miyasaka, Masayuki" sort="Miyasaka, Masayuki" uniqKey="Miyasaka M" first="Masayuki" last="Miyasaka">Masayuki Miyasaka</name><name sortKey="Murai, Toshiyuki" sort="Murai, Toshiyuki" uniqKey="Murai T" first="Toshiyuki" last="Murai">Toshiyuki Murai</name><name sortKey="Stern, Robert" sort="Stern, Robert" uniqKey="Stern R" first="Robert" last="Stern">Robert Stern</name></noCountry><country name="Japon"><noRegion><name sortKey="Sugahara, Kazuki N" sort="Sugahara, Kazuki N" uniqKey="Sugahara K" first="Kazuki N" last="Sugahara">Kazuki N. Sugahara</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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