Opposite role of Kindlin-1 and Kindlin-2 in lung cancers
Lung cancer is highly heterogenous and is composed of various subtypes that are in diverse differential stages. The newly identified integrin-interacting proteins Kindlin-1 and Kindlin-2 are the activators of transmembrane receptor integrins that play important roles in cancer progression. In this r...
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| Veröffentlicht in: | PloS one 2012-11, Vol.7 (11), p.e50313 |
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| creator | Zhan, Jun Zhu, Xiang Guo, Yongqing Wang, Yunling Wang, Yuxiang Qiang, Guangliang Niu, Miaomiao Hu, Jinxia Du, Juan Li, Zhilun Cui, Jia Ma, Bo Fang, Weigang Zhang, Hongquan |
| description | Lung cancer is highly heterogenous and is composed of various subtypes that are in diverse differential stages. The newly identified integrin-interacting proteins Kindlin-1 and Kindlin-2 are the activators of transmembrane receptor integrins that play important roles in cancer progression. In this report we present the expression profiles of Kindlin-1 and Kindlin-2 in lung cancers using patient specimens and established their correlation with lung cancer progression. We found that Kindlin-1 was expressed in epithelia-derived non-small-cell lung cancer, especially in squamous cell lung cancer but expressed at low levels in poorly differentiated large cell lung cancer. However, Kindlin-2 was highly expressed in large cell lung cancer. Both Kindlin-1 and Kindlin-2 were found not expressed or expressed at very low levels in neuroendocrine-derived small cell lung cancer. Importantly, the Kindlin-1 expression level was positively correlated with the differentiation of squamous cell lung cancer. Surprisingly, we found that the very homologous Kindlin family proteins, Kindlin-1 and Kindlin-2, displayed counteracting functional roles in lung cancer cells. Ectopic expression of Kindlin-1 in non-small-cell lung cancer cells inhibited in vitro cell migration and in vivo tumor growth, while Kindlin-2 promoted these functions. Mechanistically, Kindlin-1 prohibited epithelail to mesenchymal transition in non-small-cell lung cancer cells, while Kindlin-2 enhanced epithelail to mesenchymal transition in these cells. Taken together, we demonstrated that Kindlin-1 and Kindlin-2 differentially regulate lung cancer cell progression. Further, the expression levels of Kindlin-1 might be potentially used as a marker for lung cancer differentiation and targeting Kindlin-2 might block the invasive growth of large cell lung cancer. |
| doi_str_mv | 10.1371/journal.pone.0050313 |
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The newly identified integrin-interacting proteins Kindlin-1 and Kindlin-2 are the activators of transmembrane receptor integrins that play important roles in cancer progression. In this report we present the expression profiles of Kindlin-1 and Kindlin-2 in lung cancers using patient specimens and established their correlation with lung cancer progression. We found that Kindlin-1 was expressed in epithelia-derived non-small-cell lung cancer, especially in squamous cell lung cancer but expressed at low levels in poorly differentiated large cell lung cancer. However, Kindlin-2 was highly expressed in large cell lung cancer. Both Kindlin-1 and Kindlin-2 were found not expressed or expressed at very low levels in neuroendocrine-derived small cell lung cancer. Importantly, the Kindlin-1 expression level was positively correlated with the differentiation of squamous cell lung cancer. Surprisingly, we found that the very homologous Kindlin family proteins, Kindlin-1 and Kindlin-2, displayed counteracting functional roles in lung cancer cells. Ectopic expression of Kindlin-1 in non-small-cell lung cancer cells inhibited in vitro cell migration and in vivo tumor growth, while Kindlin-2 promoted these functions. Mechanistically, Kindlin-1 prohibited epithelail to mesenchymal transition in non-small-cell lung cancer cells, while Kindlin-2 enhanced epithelail to mesenchymal transition in these cells. Taken together, we demonstrated that Kindlin-1 and Kindlin-2 differentially regulate lung cancer cell progression. Further, the expression levels of Kindlin-1 might be potentially used as a marker for lung cancer differentiation and targeting Kindlin-2 might block the invasive growth of large cell lung cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0050313</identifier><identifier>PMID: 23209705</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Animals ; Apoptosis ; Biology ; Biomarkers, Tumor ; Bladder cancer ; Blood ; Breast cancer ; Cancer ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carrier Proteins - metabolism ; Cell adhesion & migration ; Cell differentiation ; Cell migration ; Cell Movement ; Cytoskeletal Proteins - metabolism ; Differentiation ; Disease Progression ; Ectopic expression ; Education ; Embryology ; Female ; Gastric cancer ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genetic Vectors ; Histology ; Homology ; Humans ; Integrins ; Invasiveness ; Laboratories ; Lung cancer ; Lung diseases ; Lung Neoplasms - metabolism ; Lymphatic system ; Male ; Medicine ; Membrane Proteins - metabolism ; Mesenchyme ; Mesothelioma ; Metastasis ; Mice ; Mice, Inbred BALB C ; Middle Aged ; Muscle Proteins - metabolism ; Mutation ; Neoplasm Proteins - metabolism ; Neoplasm Transplantation ; Non-small cell lung cancer ; Non-small cell lung carcinoma ; Pathology ; Prostate cancer ; Proteins ; Science ; Small cell lung carcinoma ; Stomach cancer ; Thoracic surgery</subject><ispartof>PloS one, 2012-11, Vol.7 (11), p.e50313</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Zhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Zhan et al 2012 Zhan et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c730t-28cbc43a54a61891f6ab43914096c76ff708d6faf9668474995e3f4bf7e69a473</citedby><cites>FETCH-LOGICAL-c730t-28cbc43a54a61891f6ab43914096c76ff708d6faf9668474995e3f4bf7e69a473</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/PMC3510225/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3510225/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23209705$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:125824643$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><contributor>Kalinichenko, Vladimir V.</contributor><creatorcontrib>Zhan, Jun</creatorcontrib><creatorcontrib>Zhu, Xiang</creatorcontrib><creatorcontrib>Guo, Yongqing</creatorcontrib><creatorcontrib>Wang, Yunling</creatorcontrib><creatorcontrib>Wang, Yuxiang</creatorcontrib><creatorcontrib>Qiang, Guangliang</creatorcontrib><creatorcontrib>Niu, Miaomiao</creatorcontrib><creatorcontrib>Hu, Jinxia</creatorcontrib><creatorcontrib>Du, Juan</creatorcontrib><creatorcontrib>Li, Zhilun</creatorcontrib><creatorcontrib>Cui, Jia</creatorcontrib><creatorcontrib>Ma, Bo</creatorcontrib><creatorcontrib>Fang, Weigang</creatorcontrib><creatorcontrib>Zhang, Hongquan</creatorcontrib><title>Opposite role of Kindlin-1 and Kindlin-2 in lung cancers</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Lung cancer is highly heterogenous and is composed of various subtypes that are in diverse differential stages. The newly identified integrin-interacting proteins Kindlin-1 and Kindlin-2 are the activators of transmembrane receptor integrins that play important roles in cancer progression. In this report we present the expression profiles of Kindlin-1 and Kindlin-2 in lung cancers using patient specimens and established their correlation with lung cancer progression. We found that Kindlin-1 was expressed in epithelia-derived non-small-cell lung cancer, especially in squamous cell lung cancer but expressed at low levels in poorly differentiated large cell lung cancer. However, Kindlin-2 was highly expressed in large cell lung cancer. Both Kindlin-1 and Kindlin-2 were found not expressed or expressed at very low levels in neuroendocrine-derived small cell lung cancer. Importantly, the Kindlin-1 expression level was positively correlated with the differentiation of squamous cell lung cancer. Surprisingly, we found that the very homologous Kindlin family proteins, Kindlin-1 and Kindlin-2, displayed counteracting functional roles in lung cancer cells. Ectopic expression of Kindlin-1 in non-small-cell lung cancer cells inhibited in vitro cell migration and in vivo tumor growth, while Kindlin-2 promoted these functions. Mechanistically, Kindlin-1 prohibited epithelail to mesenchymal transition in non-small-cell lung cancer cells, while Kindlin-2 enhanced epithelail to mesenchymal transition in these cells. Taken together, we demonstrated that Kindlin-1 and Kindlin-2 differentially regulate lung cancer cell progression. Further, the expression levels of Kindlin-1 might be potentially used as a marker for lung cancer differentiation and targeting Kindlin-2 might block the invasive growth of large cell lung cancer.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biology</subject><subject>Biomarkers, Tumor</subject><subject>Bladder cancer</subject><subject>Blood</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cell differentiation</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Differentiation</subject><subject>Disease Progression</subject><subject>Ectopic expression</subject><subject>Education</subject><subject>Embryology</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic Vectors</subject><subject>Histology</subject><subject>Homology</subject><subject>Humans</subject><subject>Integrins</subject><subject>Invasiveness</subject><subject>Laboratories</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lymphatic system</subject><subject>Male</subject><subject>Medicine</subject><subject>Membrane Proteins - metabolism</subject><subject>Mesenchyme</subject><subject>Mesothelioma</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Middle Aged</subject><subject>Muscle Proteins - metabolism</subject><subject>Mutation</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neoplasm Transplantation</subject><subject>Non-small cell lung cancer</subject><subject>Non-small cell lung carcinoma</subject><subject>Pathology</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Science</subject><subject>Small cell lung carcinoma</subject><subject>Stomach cancer</subject><subject>Thoracic surgery</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>D8T</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLguBFx6RJ83EjLIurgwsDft2GNE1mMmaSmrR-_PvNON1hCgqSiyQnz_uSc3iL4ikEC4gofL0NY_TSLfrg9QKABiCI7hXnkKO6IjVA90_OZ8WjlLYZQoyQh8VZjWrAKWjOC7bq-5DsoMsYnC6DKT9Y3znrK1hK3x1vdWl96Ua_LpX0Ssf0uHhgpEv6ybRfFF-u336-el_drN4try5vKkURGKqaqVZhJBssCWQcGiJbjDjEgBNFiTEUsI4YaTghDFPMeaORwa2hmnCJKboonh98exeSmJpOAqIG8OzBQCaWB6ILciv6aHcy_hZBWvGnEOJayDhY5bRghtW8Y1wqrbACslVNS7lqG0Wx0RJlr-rglX7qfmxnblPpWz5p0aCasybzb6bfje1Od0r7IUo3k81fvN2IdfghUANBXe8NXkwGMXwfdRr-0eJErWXuwnoTspna2aTEJaYUAAwBy9TiL1Rend5ZlWNibK7PBK9mgswM-tewlmNKYvnp4_-zq69z9uUJu9HSDZsU3DjY4NMcxAdQxZBS1OY4OQjEPuV30xD7lIsp5Vn27HTqR9FdrNEtXxn1rg</recordid><startdate>20121129</startdate><enddate>20121129</enddate><creator>Zhan, Jun</creator><creator>Zhu, Xiang</creator><creator>Guo, Yongqing</creator><creator>Wang, Yunling</creator><creator>Wang, Yuxiang</creator><creator>Qiang, Guangliang</creator><creator>Niu, Miaomiao</creator><creator>Hu, Jinxia</creator><creator>Du, Juan</creator><creator>Li, Zhilun</creator><creator>Cui, Jia</creator><creator>Ma, Bo</creator><creator>Fang, Weigang</creator><creator>Zhang, Hongquan</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><scope>DOA</scope></search><sort><creationdate>20121129</creationdate><title>Opposite role of Kindlin-1 and Kindlin-2 in lung cancers</title><author>Zhan, Jun ; Zhu, Xiang ; Guo, Yongqing ; Wang, Yunling ; Wang, Yuxiang ; Qiang, Guangliang ; Niu, Miaomiao ; Hu, Jinxia ; Du, Juan ; Li, Zhilun ; Cui, Jia ; Ma, Bo ; Fang, Weigang ; Zhang, Hongquan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c730t-28cbc43a54a61891f6ab43914096c76ff708d6faf9668474995e3f4bf7e69a473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biology</topic><topic>Biomarkers, Tumor</topic><topic>Bladder cancer</topic><topic>Blood</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell adhesion & migration</topic><topic>Cell differentiation</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Differentiation</topic><topic>Disease Progression</topic><topic>Ectopic expression</topic><topic>Education</topic><topic>Embryology</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic Vectors</topic><topic>Histology</topic><topic>Homology</topic><topic>Humans</topic><topic>Integrins</topic><topic>Invasiveness</topic><topic>Laboratories</topic><topic>Lung cancer</topic><topic>Lung diseases</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lymphatic system</topic><topic>Male</topic><topic>Medicine</topic><topic>Membrane Proteins - metabolism</topic><topic>Mesenchyme</topic><topic>Mesothelioma</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Middle Aged</topic><topic>Muscle Proteins - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhan, Jun</au><au>Zhu, Xiang</au><au>Guo, Yongqing</au><au>Wang, Yunling</au><au>Wang, Yuxiang</au><au>Qiang, Guangliang</au><au>Niu, Miaomiao</au><au>Hu, Jinxia</au><au>Du, Juan</au><au>Li, Zhilun</au><au>Cui, Jia</au><au>Ma, Bo</au><au>Fang, Weigang</au><au>Zhang, Hongquan</au><au>Kalinichenko, Vladimir V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Opposite role of Kindlin-1 and Kindlin-2 in lung cancers</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-11-29</date><risdate>2012</risdate><volume>7</volume><issue>11</issue><spage>e50313</spage><pages>e50313-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Lung cancer is highly heterogenous and is composed of various subtypes that are in diverse differential stages. The newly identified integrin-interacting proteins Kindlin-1 and Kindlin-2 are the activators of transmembrane receptor integrins that play important roles in cancer progression. In this report we present the expression profiles of Kindlin-1 and Kindlin-2 in lung cancers using patient specimens and established their correlation with lung cancer progression. We found that Kindlin-1 was expressed in epithelia-derived non-small-cell lung cancer, especially in squamous cell lung cancer but expressed at low levels in poorly differentiated large cell lung cancer. However, Kindlin-2 was highly expressed in large cell lung cancer. Both Kindlin-1 and Kindlin-2 were found not expressed or expressed at very low levels in neuroendocrine-derived small cell lung cancer. Importantly, the Kindlin-1 expression level was positively correlated with the differentiation of squamous cell lung cancer. Surprisingly, we found that the very homologous Kindlin family proteins, Kindlin-1 and Kindlin-2, displayed counteracting functional roles in lung cancer cells. Ectopic expression of Kindlin-1 in non-small-cell lung cancer cells inhibited in vitro cell migration and in vivo tumor growth, while Kindlin-2 promoted these functions. Mechanistically, Kindlin-1 prohibited epithelail to mesenchymal transition in non-small-cell lung cancer cells, while Kindlin-2 enhanced epithelail to mesenchymal transition in these cells. Taken together, we demonstrated that Kindlin-1 and Kindlin-2 differentially regulate lung cancer cell progression. Further, the expression levels of Kindlin-1 might be potentially used as a marker for lung cancer differentiation and targeting Kindlin-2 might block the invasive growth of large cell lung cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23209705</pmid><doi>10.1371/journal.pone.0050313</doi><tpages>e50313</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-11, Vol.7 (11), p.e50313 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1350909680 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; SWEPUB Freely available online; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adult Aged Aged, 80 and over Animals Apoptosis Biology Biomarkers, Tumor Bladder cancer Blood Breast cancer Cancer Carcinoma, Non-Small-Cell Lung - metabolism Carrier Proteins - metabolism Cell adhesion & migration Cell differentiation Cell migration Cell Movement Cytoskeletal Proteins - metabolism Differentiation Disease Progression Ectopic expression Education Embryology Female Gastric cancer Gene Expression Profiling Gene Expression Regulation, Neoplastic Genetic Vectors Histology Homology Humans Integrins Invasiveness Laboratories Lung cancer Lung diseases Lung Neoplasms - metabolism Lymphatic system Male Medicine Membrane Proteins - metabolism Mesenchyme Mesothelioma Metastasis Mice Mice, Inbred BALB C Middle Aged Muscle Proteins - metabolism Mutation Neoplasm Proteins - metabolism Neoplasm Transplantation Non-small cell lung cancer Non-small cell lung carcinoma Pathology Prostate cancer Proteins Science Small cell lung carcinoma Stomach cancer Thoracic surgery |
| title | Opposite role of Kindlin-1 and Kindlin-2 in lung cancers |
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