The role of YAP1 in small cell lung cancer
Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ, also known as WWTR1) are core downstream effectors of the Hippo pathway, which is involved in diverse biological processes. The oncogenic effects of YAP and TAZ in non-small cell lung cancer (NSCLC) have recent...
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| Veröffentlicht in: | Human cell : official journal of Human Cell Research Society 2022-03, Vol.35 (2), p.628-638 |
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| creator | Saito, Haruki Tenjin, Yuki Yamada, Tatsuya Kudoh, Shinji Kudo, Noritaka Sanada, Mune Sato, Younosuke Matsuo, Akira Orita, Yorihisa Ito, Takaaki |
| description | Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ, also known as WWTR1) are core downstream effectors of the Hippo pathway, which is involved in diverse biological processes. The oncogenic effects of YAP and TAZ in non-small cell lung cancer (NSCLC) have recently been reported; however, their roles in SCLC remain unclear. Immunohistochemistry (IHC) on lung cancer tissues and Western blotting (WB) on lung cancer cell lines were performed to examine the expression of YAP1. Genome editing using CRISPR/Cas9 was then used to knockout the YAP1 gene in the H69AR cell line. An RNA-sequence analysis, gene ontology (GO) analysis, WB, cell counting assay, invasion assays, and xenograft studies were conducted on these cells to investigate the biological roles of YAP1. IHC revealed that insulinoma-associated protein 1 was expressed in most cases (28 out of 32 cases), while only four cases expressed YAP1. The knockout of YAP1 in H69AR cells, a chemically induced SCLC-Y subtype, reduced cell proliferation and invasion capacity and restored drug sensitivity. Xenograft assays revealed that the knockout of YAP1 suppressed cell proliferation. Tumor tissues showed the expression of neuroendocrine markers and a low Ki-67 index. In SCLC, YAP1 plays an important role in biological functions, such as cell proliferation, EMT, drug sensitivity, and neuroendocrine differentiation. |
| doi_str_mv | 10.1007/s13577-022-00669-6 |
| format | Article |
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The oncogenic effects of YAP and TAZ in non-small cell lung cancer (NSCLC) have recently been reported; however, their roles in SCLC remain unclear. Immunohistochemistry (IHC) on lung cancer tissues and Western blotting (WB) on lung cancer cell lines were performed to examine the expression of YAP1. Genome editing using CRISPR/Cas9 was then used to knockout the YAP1 gene in the H69AR cell line. An RNA-sequence analysis, gene ontology (GO) analysis, WB, cell counting assay, invasion assays, and xenograft studies were conducted on these cells to investigate the biological roles of YAP1. IHC revealed that insulinoma-associated protein 1 was expressed in most cases (28 out of 32 cases), while only four cases expressed YAP1. The knockout of YAP1 in H69AR cells, a chemically induced SCLC-Y subtype, reduced cell proliferation and invasion capacity and restored drug sensitivity. Xenograft assays revealed that the knockout of YAP1 suppressed cell proliferation. Tumor tissues showed the expression of neuroendocrine markers and a low Ki-67 index. In SCLC, YAP1 plays an important role in biological functions, such as cell proliferation, EMT, drug sensitivity, and neuroendocrine differentiation.</description><identifier>ISSN: 1749-0774</identifier><identifier>ISSN: 0914-7470</identifier><identifier>EISSN: 1749-0774</identifier><identifier>DOI: 10.1007/s13577-022-00669-6</identifier><identifier>PMID: 35072899</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Biomedical and Life Sciences ; Carcinoma, Non-Small-Cell Lung - genetics ; Cell Biology ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; CRISPR ; Gene Expression Regulation, Neoplastic ; Genomes ; Gynecology ; Humans ; Immunohistochemistry ; Insulinoma ; Life Sciences ; Lung cancer ; Lung Neoplasms - pathology ; Non-small cell lung carcinoma ; Nucleotide sequence ; Oncology ; Reproductive Medicine ; Research Article ; Sequence analysis ; Small cell lung carcinoma ; Small Cell Lung Carcinoma - genetics ; Stem Cells ; Surgery ; Transcription ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tumor cell lines ; Tumors ; Western blotting ; Xenografts ; YAP-Signaling Proteins ; Yes-associated protein</subject><ispartof>Human cell : official journal of Human Cell Research Society, 2022-03, Vol.35 (2), p.628-638</ispartof><rights>The Author(s) under exclusive licence to Japan Human Cell Society 2022</rights><rights>2022. 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The oncogenic effects of YAP and TAZ in non-small cell lung cancer (NSCLC) have recently been reported; however, their roles in SCLC remain unclear. Immunohistochemistry (IHC) on lung cancer tissues and Western blotting (WB) on lung cancer cell lines were performed to examine the expression of YAP1. Genome editing using CRISPR/Cas9 was then used to knockout the YAP1 gene in the H69AR cell line. An RNA-sequence analysis, gene ontology (GO) analysis, WB, cell counting assay, invasion assays, and xenograft studies were conducted on these cells to investigate the biological roles of YAP1. IHC revealed that insulinoma-associated protein 1 was expressed in most cases (28 out of 32 cases), while only four cases expressed YAP1. The knockout of YAP1 in H69AR cells, a chemically induced SCLC-Y subtype, reduced cell proliferation and invasion capacity and restored drug sensitivity. Xenograft assays revealed that the knockout of YAP1 suppressed cell proliferation. Tumor tissues showed the expression of neuroendocrine markers and a low Ki-67 index. In SCLC, YAP1 plays an important role in biological functions, such as cell proliferation, EMT, drug sensitivity, and neuroendocrine differentiation.</description><subject>Biomedical and Life Sciences</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>CRISPR</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genomes</subject><subject>Gynecology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Insulinoma</subject><subject>Life Sciences</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - pathology</subject><subject>Non-small cell lung carcinoma</subject><subject>Nucleotide sequence</subject><subject>Oncology</subject><subject>Reproductive Medicine</subject><subject>Research Article</subject><subject>Sequence analysis</subject><subject>Small cell lung carcinoma</subject><subject>Small Cell Lung Carcinoma - genetics</subject><subject>Stem Cells</subject><subject>Surgery</subject><subject>Transcription</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Xenografts</subject><subject>YAP-Signaling Proteins</subject><subject>Yes-associated protein</subject><issn>1749-0774</issn><issn>0914-7470</issn><issn>1749-0774</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLAzEQx4Motla_gAdZ8CLC6uSxeRxL8QUFPdSDp5DNZuuWfdSke_Dbm7r1gQcvmcD85j_DD6FTDFcYQFwHTDMhUiAkBeBcpXwPjbFgKgUh2P6v_wgdhbACYBnj5BCNaAaCSKXG6HLx6hLf1S7pyuRl-oSTqk1CY-o6sS4-dd8uE2ta6_wxOihNHdzJrk7Q8-3NYnafzh_vHmbTeWqpUpu0MKUSpTJcgMQGGMeKcMgszbhxUhY5NtYVOXVWUUKMkCTngBnOpS2okBmdoIshd-27t96FjW6qsD3GtK7rgyacECYk5hDR8z_oqut9G6-LFCVYMlAiUmSgrO9C8K7Ua181xr9rDHprUg8mdTSpP01qHofOdtF93rjie-RLXQToAITYapfO_-z-J_YDi4R6jw</recordid><startdate>20220301</startdate><enddate>20220301</enddate><creator>Saito, Haruki</creator><creator>Tenjin, Yuki</creator><creator>Yamada, Tatsuya</creator><creator>Kudoh, Shinji</creator><creator>Kudo, Noritaka</creator><creator>Sanada, Mune</creator><creator>Sato, Younosuke</creator><creator>Matsuo, Akira</creator><creator>Orita, Yorihisa</creator><creator>Ito, Takaaki</creator><general>Springer Singapore</general><general>Springer Nature B.V</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>7X8</scope><orcidid>https://orcid.org/0000-0002-6064-9149</orcidid><orcidid>https://orcid.org/0000-0001-5528-3464</orcidid><orcidid>https://orcid.org/0000-0001-9610-0951</orcidid></search><sort><creationdate>20220301</creationdate><title>The role of YAP1 in small cell lung cancer</title><author>Saito, Haruki ; Tenjin, Yuki ; Yamada, Tatsuya ; Kudoh, Shinji ; Kudo, Noritaka ; Sanada, Mune ; Sato, Younosuke ; Matsuo, Akira ; Orita, Yorihisa ; Ito, Takaaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-daf97f9a67081a046192605c356ae88db1acedb3ec9322a782b60141b8cd37853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Biomedical and Life Sciences</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Cell Biology</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>CRISPR</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genomes</topic><topic>Gynecology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Insulinoma</topic><topic>Life Sciences</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - pathology</topic><topic>Non-small cell lung carcinoma</topic><topic>Nucleotide sequence</topic><topic>Oncology</topic><topic>Reproductive Medicine</topic><topic>Research Article</topic><topic>Sequence analysis</topic><topic>Small cell lung carcinoma</topic><topic>Small Cell Lung Carcinoma - genetics</topic><topic>Stem Cells</topic><topic>Surgery</topic><topic>Transcription</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><topic>Western blotting</topic><topic>Xenografts</topic><topic>YAP-Signaling Proteins</topic><topic>Yes-associated protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saito, Haruki</creatorcontrib><creatorcontrib>Tenjin, Yuki</creatorcontrib><creatorcontrib>Yamada, Tatsuya</creatorcontrib><creatorcontrib>Kudoh, Shinji</creatorcontrib><creatorcontrib>Kudo, Noritaka</creatorcontrib><creatorcontrib>Sanada, Mune</creatorcontrib><creatorcontrib>Sato, Younosuke</creatorcontrib><creatorcontrib>Matsuo, Akira</creatorcontrib><creatorcontrib>Orita, Yorihisa</creatorcontrib><creatorcontrib>Ito, Takaaki</creatorcontrib><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>Human cell : official journal of Human Cell Research Society</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saito, Haruki</au><au>Tenjin, Yuki</au><au>Yamada, Tatsuya</au><au>Kudoh, Shinji</au><au>Kudo, Noritaka</au><au>Sanada, Mune</au><au>Sato, Younosuke</au><au>Matsuo, Akira</au><au>Orita, Yorihisa</au><au>Ito, Takaaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of YAP1 in small cell lung cancer</atitle><jtitle>Human cell : official journal of Human Cell Research Society</jtitle><stitle>Human Cell</stitle><addtitle>Hum Cell</addtitle><date>2022-03-01</date><risdate>2022</risdate><volume>35</volume><issue>2</issue><spage>628</spage><epage>638</epage><pages>628-638</pages><issn>1749-0774</issn><issn>0914-7470</issn><eissn>1749-0774</eissn><abstract>Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ, also known as WWTR1) are core downstream effectors of the Hippo pathway, which is involved in diverse biological processes. The oncogenic effects of YAP and TAZ in non-small cell lung cancer (NSCLC) have recently been reported; however, their roles in SCLC remain unclear. Immunohistochemistry (IHC) on lung cancer tissues and Western blotting (WB) on lung cancer cell lines were performed to examine the expression of YAP1. Genome editing using CRISPR/Cas9 was then used to knockout the YAP1 gene in the H69AR cell line. An RNA-sequence analysis, gene ontology (GO) analysis, WB, cell counting assay, invasion assays, and xenograft studies were conducted on these cells to investigate the biological roles of YAP1. IHC revealed that insulinoma-associated protein 1 was expressed in most cases (28 out of 32 cases), while only four cases expressed YAP1. The knockout of YAP1 in H69AR cells, a chemically induced SCLC-Y subtype, reduced cell proliferation and invasion capacity and restored drug sensitivity. Xenograft assays revealed that the knockout of YAP1 suppressed cell proliferation. 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| subjects | Biomedical and Life Sciences Carcinoma, Non-Small-Cell Lung - genetics Cell Biology Cell growth Cell Line, Tumor Cell proliferation CRISPR Gene Expression Regulation, Neoplastic Genomes Gynecology Humans Immunohistochemistry Insulinoma Life Sciences Lung cancer Lung Neoplasms - pathology Non-small cell lung carcinoma Nucleotide sequence Oncology Reproductive Medicine Research Article Sequence analysis Small cell lung carcinoma Small Cell Lung Carcinoma - genetics Stem Cells Surgery Transcription Transcription Factors - genetics Transcription Factors - metabolism Tumor cell lines Tumors Western blotting Xenografts YAP-Signaling Proteins Yes-associated protein |
| title | The role of YAP1 in small cell lung cancer |
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