CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin
Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG) in NPC. Down-regulation of was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic e...
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| Veröffentlicht in: | International journal of biological sciences 2019, Vol.15 (9), p.1802-1815 |
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| creator | Chen, Juan Jiang, Chen Fu, Li Zhu, Cai-Lei Xiang, Yan-Qun Jiang, Ling-Xi Chen, Qian Liu, Wai Man Chen, Jin-Na Zhang, Li-Yi Liu, Ming Chen, Chao Tang, Hong Wang, Bo Tsao, Sai Wah Kwong, Dora Lai-Wan Guan, Xin-Yuan |
| description | Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG)
in NPC. Down-regulation of
was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers
could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis.
could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia.
could co-localize with adhesion molecule Integrin-β1, the expression of
was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that
could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion,
is a vital tumor suppressor in the carcinogenesis of NPC. |
| doi_str_mv | 10.7150/ijbs.34785 |
| format | Article |
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in NPC. Down-regulation of
was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers
could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis.
could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia.
could co-localize with adhesion molecule Integrin-β1, the expression of
was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that
could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion,
is a vital tumor suppressor in the carcinogenesis of NPC.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.34785</identifier><identifier>PMID: 31523184</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Antibodies ; Biopsy ; Blotting, Western ; Carcinogenesis ; Carcinogens ; Cdc42 protein ; Cell Adhesion Molecules - genetics ; Cell Adhesion Molecules - metabolism ; Cell cycle ; Cell Cycle Checkpoints - genetics ; Cell Cycle Checkpoints - physiology ; Cell growth ; Cell Line ; Cell Movement - genetics ; Cell Movement - physiology ; CHL1 protein ; Chromosome 3 ; Chromosome deletion ; Chromosomes ; Clonal deletion ; Committees ; Deactivation ; DNA Methylation - genetics ; DNA Methylation - physiology ; Ectopic expression ; Esophagus ; Filopodia ; Fluorescent Antibody Technique ; Gene expression ; Genes ; Human subjects ; Humans ; Immunoprecipitation ; Inactivation ; Integrin beta1 - metabolism ; Lamellipodia ; Lung cancer ; Markers ; Mesenchyme ; Metastases ; Metastasis ; Nasopharyngeal carcinoma ; Nasopharyngeal Carcinoma - genetics ; Nasopharyngeal Carcinoma - metabolism ; Neurofibromin 2 - metabolism ; Pathogenesis ; Promoter Regions, Genetic - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Rac1 protein ; Real-Time Polymerase Chain Reaction ; Research Paper ; RhoA protein ; RNA Interference ; Signal transduction ; Signal Transduction - genetics ; Signal Transduction - physiology ; Signaling ; Survival ; Tumor suppressor genes ; Tumors</subject><ispartof>International journal of biological sciences, 2019, Vol.15 (9), p.1802-1815</ispartof><rights>Copyright BioMed Central 2019</rights><rights>2019. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3495-c776a93b7f38912498977e82d5b4f13dfa45c85183dac8b0e2cb0585e7997b93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6743306/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6743306/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4022,27922,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31523184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Juan</creatorcontrib><creatorcontrib>Jiang, Chen</creatorcontrib><creatorcontrib>Fu, Li</creatorcontrib><creatorcontrib>Zhu, Cai-Lei</creatorcontrib><creatorcontrib>Xiang, Yan-Qun</creatorcontrib><creatorcontrib>Jiang, Ling-Xi</creatorcontrib><creatorcontrib>Chen, Qian</creatorcontrib><creatorcontrib>Liu, Wai Man</creatorcontrib><creatorcontrib>Chen, Jin-Na</creatorcontrib><creatorcontrib>Zhang, Li-Yi</creatorcontrib><creatorcontrib>Liu, Ming</creatorcontrib><creatorcontrib>Chen, Chao</creatorcontrib><creatorcontrib>Tang, Hong</creatorcontrib><creatorcontrib>Wang, Bo</creatorcontrib><creatorcontrib>Tsao, Sai Wah</creatorcontrib><creatorcontrib>Kwong, Dora Lai-Wan</creatorcontrib><creatorcontrib>Guan, Xin-Yuan</creatorcontrib><title>CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG)
in NPC. Down-regulation of
was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers
could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis.
could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia.
could co-localize with adhesion molecule Integrin-β1, the expression of
was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that
could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion,
is a vital tumor suppressor in the carcinogenesis of NPC.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Antibodies</subject><subject>Biopsy</subject><subject>Blotting, Western</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Cdc42 protein</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - genetics</subject><subject>Cell Cycle Checkpoints - physiology</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Movement - genetics</subject><subject>Cell Movement - physiology</subject><subject>CHL1 protein</subject><subject>Chromosome 3</subject><subject>Chromosome deletion</subject><subject>Chromosomes</subject><subject>Clonal deletion</subject><subject>Committees</subject><subject>Deactivation</subject><subject>DNA Methylation - genetics</subject><subject>DNA Methylation - physiology</subject><subject>Ectopic expression</subject><subject>Esophagus</subject><subject>Filopodia</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Human subjects</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Inactivation</subject><subject>Integrin beta1 - metabolism</subject><subject>Lamellipodia</subject><subject>Lung cancer</subject><subject>Markers</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Nasopharyngeal carcinoma</subject><subject>Nasopharyngeal Carcinoma - genetics</subject><subject>Nasopharyngeal Carcinoma - metabolism</subject><subject>Neurofibromin 2 - metabolism</subject><subject>Pathogenesis</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rac1 protein</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Research Paper</subject><subject>RhoA protein</subject><subject>RNA Interference</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - physiology</subject><subject>Signaling</subject><subject>Survival</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</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><recordid>eNp9kc9uEzEQxlcIREvhwgMgS9yQ0vpvbF-Qqgho1CA45G7Ner0bR1l7sXcb5WF4CR6EZ8JJS1UuSJbGmvnmNzP6quotwZeSCHzlt3W-ZFwq8aw6J5zrGaVKPX_yP6te5bzFmM2Fwi-rM0YEZUTx8-rn4mZFUJ6GIbmcXUbj1MeEuhT34wZBaFDvRsjl-Yx8QAFyHDaQDqFzsEMWkvUh9oDqA0ruBPGhQ9-X7Pbq-naNsu8C7I6pAcbNHg7ozkMBjS6BHX0MaO_LoGVJdKnwf_8ip6lfXSpdr6sXLeyye_MQL6r150_rxc1s9e3LcnG9mlnGtZhZKeegWS1bpjShXCstpVO0ETVvCWta4MIqQRRrwKoaO2prLJRwUmtZa3ZRfbzHDlPdu8a6MCbYmSH5vlxqInjzbyX4jeninZlLzhieF8D7B0CKPyaXR7ONUyqHZ0OFVpxKrOh_VQwTzBSWR9WHe5VNMefk2sc9CDZHv83Rb3Pyu4jfPd38UfrXYPYHb5Cpdg</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Chen, Juan</creator><creator>Jiang, Chen</creator><creator>Fu, Li</creator><creator>Zhu, Cai-Lei</creator><creator>Xiang, Yan-Qun</creator><creator>Jiang, Ling-Xi</creator><creator>Chen, Qian</creator><creator>Liu, Wai Man</creator><creator>Chen, Jin-Na</creator><creator>Zhang, Li-Yi</creator><creator>Liu, Ming</creator><creator>Chen, Chao</creator><creator>Tang, Hong</creator><creator>Wang, Bo</creator><creator>Tsao, Sai Wah</creator><creator>Kwong, Dora Lai-Wan</creator><creator>Guan, Xin-Yuan</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>2019</creationdate><title>CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin</title><author>Chen, Juan ; Jiang, Chen ; Fu, Li ; Zhu, Cai-Lei ; Xiang, Yan-Qun ; Jiang, Ling-Xi ; Chen, Qian ; Liu, Wai Man ; Chen, Jin-Na ; Zhang, Li-Yi ; Liu, Ming ; Chen, Chao ; Tang, Hong ; Wang, Bo ; Tsao, Sai Wah ; Kwong, Dora Lai-Wan ; Guan, Xin-Yuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3495-c776a93b7f38912498977e82d5b4f13dfa45c85183dac8b0e2cb0585e7997b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Antibodies</topic><topic>Biopsy</topic><topic>Blotting, Western</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Cdc42 protein</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints - genetics</topic><topic>Cell Cycle Checkpoints - physiology</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - physiology</topic><topic>CHL1 protein</topic><topic>Chromosome 3</topic><topic>Chromosome deletion</topic><topic>Chromosomes</topic><topic>Clonal deletion</topic><topic>Committees</topic><topic>Deactivation</topic><topic>DNA Methylation - genetics</topic><topic>DNA Methylation - physiology</topic><topic>Ectopic expression</topic><topic>Esophagus</topic><topic>Filopodia</topic><topic>Fluorescent Antibody Technique</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Human subjects</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Inactivation</topic><topic>Integrin beta1 - metabolism</topic><topic>Lamellipodia</topic><topic>Lung cancer</topic><topic>Markers</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Nasopharyngeal carcinoma</topic><topic>Nasopharyngeal Carcinoma - genetics</topic><topic>Nasopharyngeal Carcinoma - metabolism</topic><topic>Neurofibromin 2 - metabolism</topic><topic>Pathogenesis</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rac1 protein</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Research Paper</topic><topic>RhoA protein</topic><topic>RNA Interference</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - physiology</topic><topic>Signaling</topic><topic>Survival</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Juan</creatorcontrib><creatorcontrib>Jiang, Chen</creatorcontrib><creatorcontrib>Fu, Li</creatorcontrib><creatorcontrib>Zhu, Cai-Lei</creatorcontrib><creatorcontrib>Xiang, Yan-Qun</creatorcontrib><creatorcontrib>Jiang, Ling-Xi</creatorcontrib><creatorcontrib>Chen, Qian</creatorcontrib><creatorcontrib>Liu, Wai Man</creatorcontrib><creatorcontrib>Chen, Jin-Na</creatorcontrib><creatorcontrib>Zhang, Li-Yi</creatorcontrib><creatorcontrib>Liu, Ming</creatorcontrib><creatorcontrib>Chen, Chao</creatorcontrib><creatorcontrib>Tang, Hong</creatorcontrib><creatorcontrib>Wang, Bo</creatorcontrib><creatorcontrib>Tsao, Sai Wah</creatorcontrib><creatorcontrib>Kwong, Dora Lai-Wan</creatorcontrib><creatorcontrib>Guan, Xin-Yuan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Juan</au><au>Jiang, Chen</au><au>Fu, Li</au><au>Zhu, Cai-Lei</au><au>Xiang, Yan-Qun</au><au>Jiang, Ling-Xi</au><au>Chen, Qian</au><au>Liu, Wai Man</au><au>Chen, Jin-Na</au><au>Zhang, Li-Yi</au><au>Liu, Ming</au><au>Chen, Chao</au><au>Tang, Hong</au><au>Wang, Bo</au><au>Tsao, Sai Wah</au><au>Kwong, Dora Lai-Wan</au><au>Guan, Xin-Yuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin</atitle><jtitle>International journal of biological sciences</jtitle><addtitle>Int J Biol Sci</addtitle><date>2019</date><risdate>2019</risdate><volume>15</volume><issue>9</issue><spage>1802</spage><epage>1815</epage><pages>1802-1815</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>Deletion of Chromosome 3p is one of the most frequently detected genetic alterations in nasopharyngeal carcinoma (NPC). We reported the role of a novel 3p26.3 tumor suppressor gene (TSG)
in NPC. Down-regulation of
was detected in 4/6 of NPC cell lines and 71/95 (74.7%) in clinical tissues. Ectopic expressions of CHL1 in NPC cells significantly inhibit colony formation and cell motility in functional study. By up-regulating epithelial markers and down-regulating mesenchymal markers
could induce mesenchymal-epithelial transition (MET), a key step in preventing tumor invasion and metastasis.
could also cause the inactivation of RhoA/Rac1/Cdc42 signaling pathway and inhibit the formation of stress fiber, lamellipodia, and filopodia.
could co-localize with adhesion molecule Integrin-β1, the expression of
was positively correlated with Integrin-β1 and another known tumor suppressor gene (TSG) Merlin. Down-regulation of Integrin-β1 or Merlin was significantly correlated with the poor survival rate of NPC patients. Further mechanistic studies showed that
could directly interact with integrin-β1 and link to Merlin, leading to the inactivation of integrin β1-AKT pathway. In conclusion,
is a vital tumor suppressor in the carcinogenesis of NPC.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>31523184</pmid><doi>10.7150/ijbs.34785</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Antibodies Biopsy Blotting, Western Carcinogenesis Carcinogens Cdc42 protein Cell Adhesion Molecules - genetics Cell Adhesion Molecules - metabolism Cell cycle Cell Cycle Checkpoints - genetics Cell Cycle Checkpoints - physiology Cell growth Cell Line Cell Movement - genetics Cell Movement - physiology CHL1 protein Chromosome 3 Chromosome deletion Chromosomes Clonal deletion Committees Deactivation DNA Methylation - genetics DNA Methylation - physiology Ectopic expression Esophagus Filopodia Fluorescent Antibody Technique Gene expression Genes Human subjects Humans Immunoprecipitation Inactivation Integrin beta1 - metabolism Lamellipodia Lung cancer Markers Mesenchyme Metastases Metastasis Nasopharyngeal carcinoma Nasopharyngeal Carcinoma - genetics Nasopharyngeal Carcinoma - metabolism Neurofibromin 2 - metabolism Pathogenesis Promoter Regions, Genetic - genetics Proto-Oncogene Proteins c-akt - metabolism Rac1 protein Real-Time Polymerase Chain Reaction Research Paper RhoA protein RNA Interference Signal transduction Signal Transduction - genetics Signal Transduction - physiology Signaling Survival Tumor suppressor genes Tumors |
| title | CHL1 suppresses tumor growth and metastasis in nasopharyngeal carcinoma by repressing PI3K/AKT signaling pathway via interaction with Integrin β1 and Merlin |
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