Platelet-activating factor podoplanin: from discovery to drug development
Identifieur interne : 000296 ( Main/Exploration ); précédent : 000295; suivant : 000297Platelet-activating factor podoplanin: from discovery to drug development
Auteurs : Ai Takemoto ; Kenichi Miyata ; Naoya FujitaSource :
- Cancer Metastasis Reviews [ 0167-7659 ] ; 2017.
Abstract
Tumor cell-induced platelet aggregation facilitates hematogenous metastasis by promoting tumor embolization, preventing immunological assaults and shear stress, and the platelet-releasing growth factors support tumor growth and invasion. Podoplanin, also known as Aggrus, is a type I transmembrane mucin-like glycoprotein and is expressed on wide range of tumor cells. Podoplanin has a role in platelet aggregation and metastasis formation through the binding to its platelet receptor, C-type lectin-like receptor 2 (CLEC-2). The podoplanin research was originally started from the cloning of highly metastatic NL-17 subclone from mouse colon 26 cancer cell line and from the establishment of 8F11 monoclonal antibody (mAb) that could neutralize NL-17-induced platelet aggregation and hematogenous metastasis. Later on, podoplanin was identified as the antigen of 8F11 mAb, and its ectopic expression brought to cells the platelet-aggregating abilities and hematogenous metastasis phenotypes. From the 8F11 mAb recognition epitopes, podoplanin is found to contain tandemly repeated, highly conserved motifs, designated platelet aggregation-stimulating (PLAG) domains. Series of analyses using the cells expressing the mutants and the established neutralizing anti-podoplanin mAbs uncovered that both PLAG3 and PLAG4 domains are associated with the CLEC-2 binding. The neutralizing mAbs targeting PLAG3 or PLAG4 could suppress podoplanin-induced platelet aggregation and hematogenous metastasis through inhibiting the podoplanin–CLEC-2 binding. Therefore, these domains are certainly functional in podoplanin-mediated metastasis through its platelet-aggregating activity. This review summarizes the platelet functions in metastasis formation, the role of platelet aggregation-inducing factor podoplanin in pathological and physiological situations, and the possibility to develop podoplanin-targeting drugs in the future.
Url:
DOI: 10.1007/s10555-017-9672-2
PubMed: 28674748
PubMed Central: 5557876
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Platelet-activating factor podoplanin: from discovery to drug development</title><author><name sortKey="Takemoto, Ai" sort="Takemoto, Ai" uniqKey="Takemoto A" first="Ai" last="Takemoto">Ai Takemoto</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Miyata, Kenichi" sort="Miyata, Kenichi" uniqKey="Miyata K" first="Kenichi" last="Miyata">Kenichi Miyata</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Fujita, Naoya" sort="Fujita, Naoya" uniqKey="Fujita N" first="Naoya" last="Fujita">Naoya Fujita</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">28674748</idno><idno type="pmc">5557876</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557876</idno><idno type="RBID">PMC:5557876</idno><idno type="doi">10.1007/s10555-017-9672-2</idno><date when="2017">2017</date><idno type="wicri:Area/Pmc/Corpus">000D12</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000D12</idno><idno type="wicri:Area/Pmc/Curation">000D11</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000D11</idno><idno type="wicri:Area/Pmc/Checkpoint">000142</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000142</idno><idno type="wicri:Area/Ncbi/Merge">009241</idno><idno type="wicri:Area/Ncbi/Curation">009241</idno><idno type="wicri:Area/Ncbi/Checkpoint">009241</idno><idno type="wicri:doubleKey">0167-7659:2017:Takemoto A:platelet:activating:factor</idno><idno type="wicri:Area/Main/Merge">000296</idno><idno type="wicri:Area/Main/Curation">000296</idno><idno type="wicri:Area/Main/Exploration">000296</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Platelet-activating factor podoplanin: from discovery to drug development</title><author><name sortKey="Takemoto, Ai" sort="Takemoto, Ai" uniqKey="Takemoto A" first="Ai" last="Takemoto">Ai Takemoto</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Miyata, Kenichi" sort="Miyata, Kenichi" uniqKey="Miyata K" first="Kenichi" last="Miyata">Kenichi Miyata</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Fujita, Naoya" sort="Fujita, Naoya" uniqKey="Fujita N" first="Naoya" last="Fujita">Naoya Fujita</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Cancer Metastasis Reviews</title><idno type="ISSN">0167-7659</idno><idno type="eISSN">1573-7233</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Tumor cell-induced platelet aggregation facilitates hematogenous metastasis by promoting tumor embolization, preventing immunological assaults and shear stress, and the platelet-releasing growth factors support tumor growth and invasion. Podoplanin, also known as Aggrus, is a type I transmembrane mucin-like glycoprotein and is expressed on wide range of tumor cells. Podoplanin has a role in platelet aggregation and metastasis formation through the binding to its platelet receptor, C-type lectin-like receptor 2 (CLEC-2). The podoplanin research was originally started from the cloning of highly metastatic NL-17 subclone from mouse colon 26 cancer cell line and from the establishment of 8F11 monoclonal antibody (mAb) that could neutralize NL-17-induced platelet aggregation and hematogenous metastasis. Later on, podoplanin was identified as the antigen of 8F11 mAb, and its ectopic expression brought to cells the platelet-aggregating abilities and hematogenous metastasis phenotypes. From the 8F11 mAb recognition epitopes, podoplanin is found to contain tandemly repeated, highly conserved motifs, designated platelet aggregation-stimulating (PLAG) domains. Series of analyses using the cells expressing the mutants and the established neutralizing anti-podoplanin mAbs uncovered that both PLAG3 and PLAG4 domains are associated with the CLEC-2 binding. The neutralizing mAbs targeting PLAG3 or PLAG4 could suppress podoplanin-induced platelet aggregation and hematogenous metastasis through inhibiting the podoplanin–CLEC-2 binding. Therefore, these domains are certainly functional in podoplanin-mediated metastasis through its platelet-aggregating activity. This review summarizes the platelet functions in metastasis formation, the role of platelet aggregation-inducing factor podoplanin in pathological and physiological situations, and the possibility to develop podoplanin-targeting drugs in the future.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Menter, Dg" uniqKey="Menter D">DG Menter</name></author><author><name sortKey="Tucker, Sc" uniqKey="Tucker S">SC Tucker</name></author><author><name sortKey="Kopetz, S" uniqKey="Kopetz S">S Kopetz</name></author><author><name sortKey="Sood, Ak" uniqKey="Sood A">AK Sood</name></author><author><name sortKey="Crissman, Jd" uniqKey="Crissman J">JD Crissman</name></author><author><name sortKey="Honn, Kv" uniqKey="Honn K">KV Honn</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gay, Lj" uniqKey="Gay L">LJ Gay</name></author><author><name sortKey="Felding Habermann, B" uniqKey="Felding Habermann B">B 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H">H Oki</name></author><author><name sortKey="Ogasawara, S" uniqKey="Ogasawara S">S Ogasawara</name></author><author><name sortKey="Takagi, M" uniqKey="Takagi M">M Takagi</name></author><author><name sortKey="Kato, Y" uniqKey="Kato Y">Y Kato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chang, Yw" uniqKey="Chang Y">YW Chang</name></author><author><name sortKey="Hsieh, Pw" uniqKey="Hsieh P">PW Hsieh</name></author><author><name sortKey="Chang, Yt" uniqKey="Chang Y">YT Chang</name></author><author><name sortKey="Lu, Mh" uniqKey="Lu M">MH Lu</name></author><author><name sortKey="Huang, Tf" uniqKey="Huang T">TF Huang</name></author><author><name sortKey="Chong, Ky" uniqKey="Chong K">KY Chong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shirai, T" uniqKey="Shirai T">T Shirai</name></author><author><name sortKey="Inoue, O" uniqKey="Inoue O">O Inoue</name></author><author><name sortKey="Tamura, S" uniqKey="Tamura S">S Tamura</name></author><author><name sortKey="Tsukiji, N" uniqKey="Tsukiji N">N Tsukiji</name></author><author><name sortKey="Sasaki, T" uniqKey="Sasaki T">T Sasaki</name></author><author><name sortKey="Endo, H" uniqKey="Endo H">H Endo</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Fujita, Naoya" sort="Fujita, Naoya" uniqKey="Fujita N" first="Naoya" last="Fujita">Naoya Fujita</name><name sortKey="Miyata, Kenichi" sort="Miyata, Kenichi" uniqKey="Miyata K" first="Kenichi" last="Miyata">Kenichi Miyata</name><name sortKey="Takemoto, Ai" sort="Takemoto, Ai" uniqKey="Takemoto A" first="Ai" last="Takemoto">Ai Takemoto</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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