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High mobility group box‐1‐inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma
Melanoma inhibitory activity (MIA) is an 11‐kDa secretory protein isolated from malignant melanoma cells that is correlated with invasion and metastasis in various human malignancies. We examined MIA expression in 62 oral squamous cell carcinomas (OSCC) by immunohistochemistry. MIA expression was si...
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Published in: | Cancer science 2008-09, Vol.99 (9), p.1806-1812 |
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creator | Sasahira, Tomonori Kirita, Tadaaki Oue, Naohide Bhawal, Ujjal Kumar Yamamoto, Kazuhiko Fujii, Kiyomu Ohmori, Hitoshi Luo, Yi Yasui, Wataru Bosserhoff, Anja Katrin Kuniyasu, Hiroki |
description | Melanoma inhibitory activity (MIA) is an 11‐kDa secretory protein isolated from malignant melanoma cells that is correlated with invasion and metastasis in various human malignancies. We examined MIA expression in 62 oral squamous cell carcinomas (OSCC) by immunohistochemistry. MIA expression was significantly associated with nodal metastasis (P = 0.00018). MIA expression was also associated with expression of high mobility group box‐1 (HMGB1) (P |
doi_str_mv | 10.1111/j.1349-7006.2008.00894.x |
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We examined MIA expression in 62 oral squamous cell carcinomas (OSCC) by immunohistochemistry. MIA expression was significantly associated with nodal metastasis (P = 0.00018). MIA expression was also associated with expression of high mobility group box‐1 (HMGB1) (P < 0.0001) and lymph vessel density (P < 0.0001). Expression levels of MIA, HMGB1, nuclear factor kB (NFkB) p65 and HMGB1–NFkB p65 binding were significantly higher in a metastatic human OSCC cell line (HSC3) than those in a non‐metastatic OSCC cell line (HSC4). Treatment with receptor for advanced glycation end products (RAGE) antisense or small interfering RNA and human recombinant HMGB1 (hrHMGB1) did not affect MIA expression, whereas HMGB1 antisense or siRNA treatment decreased MIA expression in HSC3 cells. Then HMGB1 enhanced MIA expression as an NFkB cofactor but not as a RAGE ligand. MIA neutralization by MIA antibodies increased extracellular signal‐related kinase 1/2 phosphorylation, but decreased p38 phosphorylation and the expression of vascular epithelial growth factor (VEGF)‐C and ‐D. Treatment with p38 inihibitor decreased VEGF‐C and ‐D expression in HSC3 cells. These results suggest that MIA expression is enhanced by the interaction of intracellular HMGB1 and NFkBp65 and MIA is closely involved in tumor progression and nodal metastasis by the increments of VEGF‐C and VEGF‐D in OSCC. 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Myelofibrosis ; Lymphangiogenesis ; Lymphatic Metastasis ; Male ; Medical sciences ; Middle Aged ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; Neoplasm Proteins ; NF-kappa B - metabolism ; Original ; Transcription Factor RelA - metabolism ; Tumors ; Vascular Endothelial Growth Factor C - metabolism ; Vascular Endothelial Growth Factor D - metabolism</subject><ispartof>Cancer science, 2008-09, Vol.99 (9), p.1806-1812</ispartof><rights>2008 Japanese Cancer Association</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5864-1fd733760bd5be056b7f8ce0482a94cd0b87388141cea7ed2b3f2a05d3feb9e33</citedby><cites>FETCH-LOGICAL-c5864-1fd733760bd5be056b7f8ce0482a94cd0b87388141cea7ed2b3f2a05d3feb9e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11159509/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11159509/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,11562,27924,27925,37013,46052,46476,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1349-7006.2008.00894.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20697886$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18616526$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sasahira, Tomonori</creatorcontrib><creatorcontrib>Kirita, Tadaaki</creatorcontrib><creatorcontrib>Oue, Naohide</creatorcontrib><creatorcontrib>Bhawal, Ujjal Kumar</creatorcontrib><creatorcontrib>Yamamoto, Kazuhiko</creatorcontrib><creatorcontrib>Fujii, Kiyomu</creatorcontrib><creatorcontrib>Ohmori, Hitoshi</creatorcontrib><creatorcontrib>Luo, Yi</creatorcontrib><creatorcontrib>Yasui, Wataru</creatorcontrib><creatorcontrib>Bosserhoff, Anja Katrin</creatorcontrib><creatorcontrib>Kuniyasu, Hiroki</creatorcontrib><title>High mobility group box‐1‐inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Melanoma inhibitory activity (MIA) is an 11‐kDa secretory protein isolated from malignant melanoma cells that is correlated with invasion and metastasis in various human malignancies. We examined MIA expression in 62 oral squamous cell carcinomas (OSCC) by immunohistochemistry. MIA expression was significantly associated with nodal metastasis (P = 0.00018). MIA expression was also associated with expression of high mobility group box‐1 (HMGB1) (P < 0.0001) and lymph vessel density (P < 0.0001). Expression levels of MIA, HMGB1, nuclear factor kB (NFkB) p65 and HMGB1–NFkB p65 binding were significantly higher in a metastatic human OSCC cell line (HSC3) than those in a non‐metastatic OSCC cell line (HSC4). Treatment with receptor for advanced glycation end products (RAGE) antisense or small interfering RNA and human recombinant HMGB1 (hrHMGB1) did not affect MIA expression, whereas HMGB1 antisense or siRNA treatment decreased MIA expression in HSC3 cells. Then HMGB1 enhanced MIA expression as an NFkB cofactor but not as a RAGE ligand. MIA neutralization by MIA antibodies increased extracellular signal‐related kinase 1/2 phosphorylation, but decreased p38 phosphorylation and the expression of vascular epithelial growth factor (VEGF)‐C and ‐D. Treatment with p38 inihibitor decreased VEGF‐C and ‐D expression in HSC3 cells. These results suggest that MIA expression is enhanced by the interaction of intracellular HMGB1 and NFkBp65 and MIA is closely involved in tumor progression and nodal metastasis by the increments of VEGF‐C and VEGF‐D in OSCC. 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Myelofibrosis</subject><subject>Lymphangiogenesis</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mouth Neoplasms - metabolism</subject><subject>Mouth Neoplasms - pathology</subject><subject>Neoplasm Proteins</subject><subject>NF-kappa B - metabolism</subject><subject>Original</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Tumors</subject><subject>Vascular Endothelial Growth Factor C - metabolism</subject><subject>Vascular Endothelial Growth Factor D - metabolism</subject><issn>1347-9032</issn><issn>1349-7006</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqNkt2O1CAYhhujcdfVWzCc6FkrlJZCYmI2k9U12cQD9ZgApe03aWG2tLvTMy_BK_DivBLpzmTUIyUQCDzv95OXJEEEZySON9uM0EKkFcYsyzHmWVyiyPaPkvPTw-OHc5UKTPOz5FkIW4wpK0TxNDkjnBFW5uw8-XENbYcGr6GHaUHt6Ocd0n7_89t3Ehe4ejage4sG2yvnB4XAdaBh8uOClJngbpVBQCoEb0BNtkb3MHXI-Vr1UTWpEOcKuBr1y7DrlGvBt9bZ9RYc8mMEw-2sBj8HZGzfI6NGA2u258mTRvXBvjjuF8nX91dfNtfpzacPHzeXN6kpOStS0tQVpRXDui61xSXTVcONxQXPlShMjTWvKOekIMaqyta5pk2ucFnTxmphKb1I3h3i7mY92NpYN8Wq5G6EQY2L9Ark3y8OOtn6OxndKEWJRYzw-hhh9LezDZMcIKzNKGdjX5IJhitM8n-C0c9ciKqMID-AZvQhjLY5lUPwmpfIrVzdlqvbq4zLh28g91H68s92fguPvkfg1RFQwai-GZUzEE5cjpmoOF-5twfuHnq7_HcBcnP5OR7oLxX01Zc</recordid><startdate>200809</startdate><enddate>200809</enddate><creator>Sasahira, Tomonori</creator><creator>Kirita, Tadaaki</creator><creator>Oue, Naohide</creator><creator>Bhawal, Ujjal Kumar</creator><creator>Yamamoto, Kazuhiko</creator><creator>Fujii, Kiyomu</creator><creator>Ohmori, Hitoshi</creator><creator>Luo, Yi</creator><creator>Yasui, Wataru</creator><creator>Bosserhoff, Anja Katrin</creator><creator>Kuniyasu, Hiroki</creator><general>Blackwell Publishing Asia</general><general>Blackwell</general><scope>IQODW</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>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200809</creationdate><title>High mobility group box‐1‐inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma</title><author>Sasahira, Tomonori ; Kirita, Tadaaki ; Oue, Naohide ; Bhawal, Ujjal Kumar ; Yamamoto, Kazuhiko ; Fujii, Kiyomu ; Ohmori, Hitoshi ; Luo, Yi ; Yasui, Wataru ; Bosserhoff, Anja Katrin ; Kuniyasu, Hiroki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5864-1fd733760bd5be056b7f8ce0482a94cd0b87388141cea7ed2b3f2a05d3feb9e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Biological and medical sciences</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hematologic and hematopoietic diseases</topic><topic>HMGB Proteins - metabolism</topic><topic>HMGB1 Protein - metabolism</topic><topic>Humans</topic><topic>Leukemias. 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Myelofibrosis</topic><topic>Lymphangiogenesis</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mouth Neoplasms - metabolism</topic><topic>Mouth Neoplasms - pathology</topic><topic>Neoplasm Proteins</topic><topic>NF-kappa B - metabolism</topic><topic>Original</topic><topic>Transcription Factor RelA - metabolism</topic><topic>Tumors</topic><topic>Vascular Endothelial Growth Factor C - metabolism</topic><topic>Vascular Endothelial Growth Factor D - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sasahira, Tomonori</creatorcontrib><creatorcontrib>Kirita, Tadaaki</creatorcontrib><creatorcontrib>Oue, Naohide</creatorcontrib><creatorcontrib>Bhawal, Ujjal Kumar</creatorcontrib><creatorcontrib>Yamamoto, Kazuhiko</creatorcontrib><creatorcontrib>Fujii, Kiyomu</creatorcontrib><creatorcontrib>Ohmori, Hitoshi</creatorcontrib><creatorcontrib>Luo, Yi</creatorcontrib><creatorcontrib>Yasui, Wataru</creatorcontrib><creatorcontrib>Bosserhoff, Anja Katrin</creatorcontrib><creatorcontrib>Kuniyasu, Hiroki</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</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_linktorsrc</fulltext></delivery><addata><au>Sasahira, Tomonori</au><au>Kirita, Tadaaki</au><au>Oue, Naohide</au><au>Bhawal, Ujjal Kumar</au><au>Yamamoto, Kazuhiko</au><au>Fujii, Kiyomu</au><au>Ohmori, Hitoshi</au><au>Luo, Yi</au><au>Yasui, Wataru</au><au>Bosserhoff, Anja Katrin</au><au>Kuniyasu, Hiroki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High mobility group box‐1‐inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2008-09</date><risdate>2008</risdate><volume>99</volume><issue>9</issue><spage>1806</spage><epage>1812</epage><pages>1806-1812</pages><issn>1347-9032</issn><issn>1349-7006</issn><eissn>1349-7006</eissn><abstract>Melanoma inhibitory activity (MIA) is an 11‐kDa secretory protein isolated from malignant melanoma cells that is correlated with invasion and metastasis in various human malignancies. We examined MIA expression in 62 oral squamous cell carcinomas (OSCC) by immunohistochemistry. MIA expression was significantly associated with nodal metastasis (P = 0.00018). MIA expression was also associated with expression of high mobility group box‐1 (HMGB1) (P < 0.0001) and lymph vessel density (P < 0.0001). Expression levels of MIA, HMGB1, nuclear factor kB (NFkB) p65 and HMGB1–NFkB p65 binding were significantly higher in a metastatic human OSCC cell line (HSC3) than those in a non‐metastatic OSCC cell line (HSC4). Treatment with receptor for advanced glycation end products (RAGE) antisense or small interfering RNA and human recombinant HMGB1 (hrHMGB1) did not affect MIA expression, whereas HMGB1 antisense or siRNA treatment decreased MIA expression in HSC3 cells. Then HMGB1 enhanced MIA expression as an NFkB cofactor but not as a RAGE ligand. MIA neutralization by MIA antibodies increased extracellular signal‐related kinase 1/2 phosphorylation, but decreased p38 phosphorylation and the expression of vascular epithelial growth factor (VEGF)‐C and ‐D. Treatment with p38 inihibitor decreased VEGF‐C and ‐D expression in HSC3 cells. These results suggest that MIA expression is enhanced by the interaction of intracellular HMGB1 and NFkBp65 and MIA is closely involved in tumor progression and nodal metastasis by the increments of VEGF‐C and VEGF‐D in OSCC. (Cancer Sci 2008; 99: 1806– 1812)</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>18616526</pmid><doi>10.1111/j.1349-7006.2008.00894.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biological and medical sciences Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Extracellular Matrix Proteins - metabolism Female Gene Expression Regulation, Neoplastic Hematologic and hematopoietic diseases HMGB Proteins - metabolism HMGB1 Protein - metabolism Humans Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphangiogenesis Lymphatic Metastasis Male Medical sciences Middle Aged Mouth Neoplasms - metabolism Mouth Neoplasms - pathology Neoplasm Proteins NF-kappa B - metabolism Original Transcription Factor RelA - metabolism Tumors Vascular Endothelial Growth Factor C - metabolism Vascular Endothelial Growth Factor D - metabolism |
title | High mobility group box‐1‐inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma |
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