Immunohistochemical study of Skp2 and Jab1, two key molecules in the degradation of P27, in lung adenocarcinoma
To clarify the association of the P27 degradation pathway proteins, Skp2 and Jab1, with the development and progression of lung adenocarcinoma (AD), we immunohistochemically investigated Skp2 and Jab1 expression together with P27‐ and Ki‐67‐labeling in 110 lung AD and 11 atypical adenomatous hyperpl...
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| Veröffentlicht in: | Pathology international 2004-09, Vol.54 (9), p.675-681 |
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| creator | Goto, Akiteru Niki, Toshiro Moriyama, Sachiko Funata, Nobuaki Moriyama, Hirokazu Nishimura, Yoshihiro Tsuchida, Rika Kato, Jun-ya Fukayama, Masashi |
| description | To clarify the association of the P27 degradation pathway proteins, Skp2 and Jab1, with the development and progression of lung adenocarcinoma (AD), we immunohistochemically investigated Skp2 and Jab1 expression together with P27‐ and Ki‐67‐labeling in 110 lung AD and 11 atypical adenomatous hyperplasia (AAH) and analyzed the relationship between the expression of these proteins and the clinicopathological factors. High Skp2 or Jab1 expression was frequent in lung AD (52/110, 47%, and 59/110, 54%, respectively), and high expression of Jab1 was also frequent in AAH (4/11, 36%), while it was not observed in normal bronchiolar epithelium. The P27 labeling index (LI) was reciprocally correlated with high Skp2 and Jab1 expression, and a higher Ki‐67 LI was significantly correlated with high Skp2 and Jab1 expression. However, low P27 expression did not correlate with a higher Ki‐67 LI. High Skp2 lung AD showed significant correlation with blood and lymphatic vessel invasion, which low P27 expression did not correlate with. Furthermore, high Skp2 expression in lung AD was significantly correlated with a poor outcome for patients. Thus, Skp2 and Jab1 regulate P27 degradation, and might contribute to the development and progression of lung AD through P27‐mediated and –unmediated mechanisms. |
| doi_str_mv | 10.1111/j.1440-1827.2004.01679.x |
| format | Article |
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High Skp2 or Jab1 expression was frequent in lung AD (52/110, 47%, and 59/110, 54%, respectively), and high expression of Jab1 was also frequent in AAH (4/11, 36%), while it was not observed in normal bronchiolar epithelium. The P27 labeling index (LI) was reciprocally correlated with high Skp2 and Jab1 expression, and a higher Ki‐67 LI was significantly correlated with high Skp2 and Jab1 expression. However, low P27 expression did not correlate with a higher Ki‐67 LI. High Skp2 lung AD showed significant correlation with blood and lymphatic vessel invasion, which low P27 expression did not correlate with. Furthermore, high Skp2 expression in lung AD was significantly correlated with a poor outcome for patients. Thus, Skp2 and Jab1 regulate P27 degradation, and might contribute to the development and progression of lung AD through P27‐mediated and –unmediated mechanisms.</description><identifier>ISSN: 1320-5463</identifier><identifier>EISSN: 1440-1827</identifier><identifier>DOI: 10.1111/j.1440-1827.2004.01679.x</identifier><identifier>PMID: 15363035</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Science Pty</publisher><subject>Adenocarcinoma - metabolism ; Adenocarcinoma - mortality ; Adenocarcinoma - secondary ; Adult ; Aged ; Aged, 80 and over ; atypical adenomatous hyperplasia ; Biomarkers, Tumor - metabolism ; Cell Count ; Cell Cycle Proteins - metabolism ; COP9 Signalosome Complex ; Cyclin-Dependent Kinase Inhibitor p27 ; Disease Progression ; DNA-Binding Proteins - metabolism ; Female ; Humans ; Immunoenzyme Techniques ; Intracellular Signaling Peptides and Proteins ; Jab1 ; Japan - epidemiology ; Ki-67 ; Ki-67 Antigen - metabolism ; lung adenocarcinoma ; Lung Neoplasms - metabolism ; Lung Neoplasms - mortality ; Lung Neoplasms - pathology ; Male ; Middle Aged ; Neoplasm Staging ; P27 (kip1) ; Peptide Hydrolases ; prognosis ; S-Phase Kinase-Associated Proteins - metabolism ; Skp2 ; Survival Rate ; Transcription Factors - metabolism ; Tumor Suppressor Proteins - metabolism</subject><ispartof>Pathology international, 2004-09, Vol.54 (9), p.675-681</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4569-b4f94b1eb0e3a81b2f56b1dbc73a77af0846cb15dc365a3a46801ddc9a56e4303</citedby><cites>FETCH-LOGICAL-c4569-b4f94b1eb0e3a81b2f56b1dbc73a77af0846cb15dc365a3a46801ddc9a56e4303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1440-1827.2004.01679.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1440-1827.2004.01679.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15363035$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goto, Akiteru</creatorcontrib><creatorcontrib>Niki, Toshiro</creatorcontrib><creatorcontrib>Moriyama, Sachiko</creatorcontrib><creatorcontrib>Funata, Nobuaki</creatorcontrib><creatorcontrib>Moriyama, Hirokazu</creatorcontrib><creatorcontrib>Nishimura, Yoshihiro</creatorcontrib><creatorcontrib>Tsuchida, Rika</creatorcontrib><creatorcontrib>Kato, Jun-ya</creatorcontrib><creatorcontrib>Fukayama, Masashi</creatorcontrib><title>Immunohistochemical study of Skp2 and Jab1, two key molecules in the degradation of P27, in lung adenocarcinoma</title><title>Pathology international</title><addtitle>Pathol Int</addtitle><description>To clarify the association of the P27 degradation pathway proteins, Skp2 and Jab1, with the development and progression of lung adenocarcinoma (AD), we immunohistochemically investigated Skp2 and Jab1 expression together with P27‐ and Ki‐67‐labeling in 110 lung AD and 11 atypical adenomatous hyperplasia (AAH) and analyzed the relationship between the expression of these proteins and the clinicopathological factors. High Skp2 or Jab1 expression was frequent in lung AD (52/110, 47%, and 59/110, 54%, respectively), and high expression of Jab1 was also frequent in AAH (4/11, 36%), while it was not observed in normal bronchiolar epithelium. The P27 labeling index (LI) was reciprocally correlated with high Skp2 and Jab1 expression, and a higher Ki‐67 LI was significantly correlated with high Skp2 and Jab1 expression. However, low P27 expression did not correlate with a higher Ki‐67 LI. High Skp2 lung AD showed significant correlation with blood and lymphatic vessel invasion, which low P27 expression did not correlate with. Furthermore, high Skp2 expression in lung AD was significantly correlated with a poor outcome for patients. Thus, Skp2 and Jab1 regulate P27 degradation, and might contribute to the development and progression of lung AD through P27‐mediated and –unmediated mechanisms.</description><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - mortality</subject><subject>Adenocarcinoma - secondary</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>atypical adenomatous hyperplasia</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cell Count</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>COP9 Signalosome Complex</subject><subject>Cyclin-Dependent Kinase Inhibitor p27</subject><subject>Disease Progression</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Jab1</subject><subject>Japan - epidemiology</subject><subject>Ki-67</subject><subject>Ki-67 Antigen - metabolism</subject><subject>lung adenocarcinoma</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - mortality</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neoplasm Staging</subject><subject>P27 (kip1)</subject><subject>Peptide Hydrolases</subject><subject>prognosis</subject><subject>S-Phase Kinase-Associated Proteins - metabolism</subject><subject>Skp2</subject><subject>Survival Rate</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor Suppressor Proteins - metabolism</subject><issn>1320-5463</issn><issn>1440-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhiMEoh_wF5BPnJpgx1_JgQOsaFmolkqAOFpje9LNbhIvcaLu_vsm7Kq94otHmveZkR8nCWE0Y9P5sMmYEDRlRa6znFKRUaZ0me1fJOdPjZdTzXOaSqH4WXIR44ZSprmir5MzJrnilMvzJCzbduzCuo5DcGtsawcNicPoDyRU5Od2lxPoPPkGll2R4SGQLR5IGxp0Y4OR1B0Z1kg83vfgYahDN2N3ub6aW83Y3RPw2AUHvau70MKb5FUFTcS3p_sy-X395dfia3r742a5-HSbOiFVmVpRlcIytBQ5FMzmlVSWees0B62hooVQzjLpHVcSOAhVUOa9K0EqFNPTLpP3x7m7PvwdMQ6mraPDpoEOwxiNUoWWkqkpWByDrg8x9liZXV-30B8Mo2aWbTZmdmpmp2aWbf7JNvsJfXfaMdoW_TN4sjsFPh4DD3WDh_8ebO6Wq7ma-PTIT7-D-yce-q1Rmmtp_qxuzOfVd1oKvjIL_giH5ZyQ</recordid><startdate>200409</startdate><enddate>200409</enddate><creator>Goto, Akiteru</creator><creator>Niki, Toshiro</creator><creator>Moriyama, Sachiko</creator><creator>Funata, Nobuaki</creator><creator>Moriyama, Hirokazu</creator><creator>Nishimura, Yoshihiro</creator><creator>Tsuchida, Rika</creator><creator>Kato, Jun-ya</creator><creator>Fukayama, Masashi</creator><general>Blackwell Science Pty</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>200409</creationdate><title>Immunohistochemical study of Skp2 and Jab1, two key molecules in the degradation of P27, in lung adenocarcinoma</title><author>Goto, Akiteru ; Niki, Toshiro ; Moriyama, Sachiko ; Funata, Nobuaki ; Moriyama, Hirokazu ; Nishimura, Yoshihiro ; Tsuchida, Rika ; Kato, Jun-ya ; Fukayama, Masashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4569-b4f94b1eb0e3a81b2f56b1dbc73a77af0846cb15dc365a3a46801ddc9a56e4303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - mortality</topic><topic>Adenocarcinoma - secondary</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>atypical adenomatous hyperplasia</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cell Count</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>COP9 Signalosome Complex</topic><topic>Cyclin-Dependent Kinase Inhibitor p27</topic><topic>Disease Progression</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>Jab1</topic><topic>Japan - epidemiology</topic><topic>Ki-67</topic><topic>Ki-67 Antigen - metabolism</topic><topic>lung adenocarcinoma</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - mortality</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neoplasm Staging</topic><topic>P27 (kip1)</topic><topic>Peptide Hydrolases</topic><topic>prognosis</topic><topic>S-Phase Kinase-Associated Proteins - metabolism</topic><topic>Skp2</topic><topic>Survival Rate</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor Suppressor Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goto, Akiteru</creatorcontrib><creatorcontrib>Niki, Toshiro</creatorcontrib><creatorcontrib>Moriyama, Sachiko</creatorcontrib><creatorcontrib>Funata, Nobuaki</creatorcontrib><creatorcontrib>Moriyama, Hirokazu</creatorcontrib><creatorcontrib>Nishimura, Yoshihiro</creatorcontrib><creatorcontrib>Tsuchida, Rika</creatorcontrib><creatorcontrib>Kato, Jun-ya</creatorcontrib><creatorcontrib>Fukayama, Masashi</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Pathology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goto, Akiteru</au><au>Niki, Toshiro</au><au>Moriyama, Sachiko</au><au>Funata, Nobuaki</au><au>Moriyama, Hirokazu</au><au>Nishimura, Yoshihiro</au><au>Tsuchida, Rika</au><au>Kato, Jun-ya</au><au>Fukayama, Masashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunohistochemical study of Skp2 and Jab1, two key molecules in the degradation of P27, in lung adenocarcinoma</atitle><jtitle>Pathology international</jtitle><addtitle>Pathol Int</addtitle><date>2004-09</date><risdate>2004</risdate><volume>54</volume><issue>9</issue><spage>675</spage><epage>681</epage><pages>675-681</pages><issn>1320-5463</issn><eissn>1440-1827</eissn><abstract>To clarify the association of the P27 degradation pathway proteins, Skp2 and Jab1, with the development and progression of lung adenocarcinoma (AD), we immunohistochemically investigated Skp2 and Jab1 expression together with P27‐ and Ki‐67‐labeling in 110 lung AD and 11 atypical adenomatous hyperplasia (AAH) and analyzed the relationship between the expression of these proteins and the clinicopathological factors. High Skp2 or Jab1 expression was frequent in lung AD (52/110, 47%, and 59/110, 54%, respectively), and high expression of Jab1 was also frequent in AAH (4/11, 36%), while it was not observed in normal bronchiolar epithelium. The P27 labeling index (LI) was reciprocally correlated with high Skp2 and Jab1 expression, and a higher Ki‐67 LI was significantly correlated with high Skp2 and Jab1 expression. However, low P27 expression did not correlate with a higher Ki‐67 LI. High Skp2 lung AD showed significant correlation with blood and lymphatic vessel invasion, which low P27 expression did not correlate with. Furthermore, high Skp2 expression in lung AD was significantly correlated with a poor outcome for patients. Thus, Skp2 and Jab1 regulate P27 degradation, and might contribute to the development and progression of lung AD through P27‐mediated and –unmediated mechanisms.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Science Pty</pub><pmid>15363035</pmid><doi>10.1111/j.1440-1827.2004.01679.x</doi><tpages>7</tpages></addata></record> |
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| ispartof | Pathology international, 2004-09, Vol.54 (9), p.675-681 |
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| subjects | Adenocarcinoma - metabolism Adenocarcinoma - mortality Adenocarcinoma - secondary Adult Aged Aged, 80 and over atypical adenomatous hyperplasia Biomarkers, Tumor - metabolism Cell Count Cell Cycle Proteins - metabolism COP9 Signalosome Complex Cyclin-Dependent Kinase Inhibitor p27 Disease Progression DNA-Binding Proteins - metabolism Female Humans Immunoenzyme Techniques Intracellular Signaling Peptides and Proteins Jab1 Japan - epidemiology Ki-67 Ki-67 Antigen - metabolism lung adenocarcinoma Lung Neoplasms - metabolism Lung Neoplasms - mortality Lung Neoplasms - pathology Male Middle Aged Neoplasm Staging P27 (kip1) Peptide Hydrolases prognosis S-Phase Kinase-Associated Proteins - metabolism Skp2 Survival Rate Transcription Factors - metabolism Tumor Suppressor Proteins - metabolism |
| title | Immunohistochemical study of Skp2 and Jab1, two key molecules in the degradation of P27, in lung adenocarcinoma |
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