Transformer 2β (Tra2β/SFRS10) positively regulates the progression of NSCLC via promoting cell proliferation
Transformer 2β (Tra2β), a member of the serine/arginine-rich-like protein family, is an important RNA-binding protein involved in alternative splice. Deregulation of Tra2β has been observed in several cancers. However, the detailed role of Tra2β in non-small cell lung cancer (NSCLC) has not been elu...
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creator | Ji, Lili Ni, Tingting Shen, Yanbo Xue, Qun Liu, Yifei Chen, Buyou Cui, Xuefan Lv, Liting Yu, Xiafei Cui, Yuan Lu, Xiaoning Chen, Jie Mao, Guoxin Wang, Yuchan |
description | Transformer 2β (Tra2β), a member of the serine/arginine-rich-like protein family, is an important RNA-binding protein involved in alternative splice. Deregulation of Tra2β has been observed in several cancers. However, the detailed role of Tra2β in non-small cell lung cancer (NSCLC) has not been elucidated. In this study, the contribution of Tra2β to NSCLC development was investigated. On histological level, the expression of Tra2β was determined by Western and immunohistochemistry assays. It demonstrated that Tra2β was expressed higher in NSCLC tumor tissues compared with adjacent non-tumor tissues. In addition to confirm the association of Tra2β expression with histological differentiation and clinical stage (
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doi_str_mv | 10.1007/s10735-014-9582-3 |
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p
< 0.05), we also confirmed significant positive correlation between the expression level of Tra2β and that of Ki67 (
p
< 0.05, r = 0.446) by Spearman rank correlation test. Moreover, high expression of Tra2β predicted poor prognosis by Kaplan–Meier survival analysis. And Tra2β among with other clinicopathologic variables was an independent prognostic indicator for patients’ overall survival by multivariate analysis. On cellular level, Tra2β expression was demonstrated to promote proliferation of NSCLC cells through a series of assays, including serum starvation and release assay, Western blot assay and flow cytometry analysis. Moreover, knockdown of Tra2β was confirmed to inhibit proliferation and to induce apoptosis of NSCLC cells through flow cytometry analysis, western analysis, cell counting kit-8 assay and Tunnel assay. Our results indicated that Tra2β was involved in the tumorigenesis of NSCLC and might be a potential therapeutic target of NSCLC.</description><identifier>ISSN: 1567-2379</identifier><identifier>EISSN: 1567-2387</identifier><identifier>DOI: 10.1007/s10735-014-9582-3</identifier><identifier>PMID: 24952301</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Biology ; Cell Line, Tumor ; Cell Proliferation ; Developmental Biology ; Disease Progression ; Female ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Ki-67 Antigen - metabolism ; Life Sciences ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Male ; Middle Aged ; Neoplasm Staging ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Original Paper ; Prognosis ; RNA Interference ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Serine-Arginine Splicing Factors</subject><ispartof>Journal of molecular histology, 2014-10, Vol.45 (5), p.573-582</ispartof><rights>Springer Science+Business Media Dordrecht 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c484t-a76905ce60f2c899ec73054af5417894af8c469ce0c053280f6aebd3bb22c3b33</citedby><cites>FETCH-LOGICAL-c484t-a76905ce60f2c899ec73054af5417894af8c469ce0c053280f6aebd3bb22c3b33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10735-014-9582-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10735-014-9582-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24952301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ji, Lili</creatorcontrib><creatorcontrib>Ni, Tingting</creatorcontrib><creatorcontrib>Shen, Yanbo</creatorcontrib><creatorcontrib>Xue, Qun</creatorcontrib><creatorcontrib>Liu, Yifei</creatorcontrib><creatorcontrib>Chen, Buyou</creatorcontrib><creatorcontrib>Cui, Xuefan</creatorcontrib><creatorcontrib>Lv, Liting</creatorcontrib><creatorcontrib>Yu, Xiafei</creatorcontrib><creatorcontrib>Cui, Yuan</creatorcontrib><creatorcontrib>Lu, Xiaoning</creatorcontrib><creatorcontrib>Chen, Jie</creatorcontrib><creatorcontrib>Mao, Guoxin</creatorcontrib><creatorcontrib>Wang, Yuchan</creatorcontrib><title>Transformer 2β (Tra2β/SFRS10) positively regulates the progression of NSCLC via promoting cell proliferation</title><title>Journal of molecular histology</title><addtitle>J Mol Hist</addtitle><addtitle>J Mol Histol</addtitle><description>Transformer 2β (Tra2β), a member of the serine/arginine-rich-like protein family, is an important RNA-binding protein involved in alternative splice. Deregulation of Tra2β has been observed in several cancers. However, the detailed role of Tra2β in non-small cell lung cancer (NSCLC) has not been elucidated. In this study, the contribution of Tra2β to NSCLC development was investigated. On histological level, the expression of Tra2β was determined by Western and immunohistochemistry assays. It demonstrated that Tra2β was expressed higher in NSCLC tumor tissues compared with adjacent non-tumor tissues. In addition to confirm the association of Tra2β expression with histological differentiation and clinical stage (
p
< 0.05), we also confirmed significant positive correlation between the expression level of Tra2β and that of Ki67 (
p
< 0.05, r = 0.446) by Spearman rank correlation test. Moreover, high expression of Tra2β predicted poor prognosis by Kaplan–Meier survival analysis. And Tra2β among with other clinicopathologic variables was an independent prognostic indicator for patients’ overall survival by multivariate analysis. On cellular level, Tra2β expression was demonstrated to promote proliferation of NSCLC cells through a series of assays, including serum starvation and release assay, Western blot assay and flow cytometry analysis. Moreover, knockdown of Tra2β was confirmed to inhibit proliferation and to induce apoptosis of NSCLC cells through flow cytometry analysis, western analysis, cell counting kit-8 assay and Tunnel assay. Our results indicated that Tra2β was involved in the tumorigenesis of NSCLC and might be a potential therapeutic target of NSCLC.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Western</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Developmental Biology</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Life Sciences</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neoplasm Staging</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Original Paper</subject><subject>Prognosis</subject><subject>RNA Interference</subject><subject>RNA-Binding Proteins - genetics</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Serine-Arginine Splicing Factors</subject><issn>1567-2379</issn><issn>1567-2387</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOxCAUhonReH8AN4alLqoHKC0szcRbMtHE0TWheDrWtGWE1sTX8kF8JmlGXbo6B87HD3yEHDE4YwDleWRQCpkByzMtFc_EBtllsigzLlS5-deXeofsxfgKwFWR622yw3MtuQC2S_rHYPtY-9BhoPzrk56kjVTPF1cPCwandOVjMzTv2H7QgMuxtQNGOrwgXQW_DBhj43vqa3q3mM1n9L2x06DzQ9MvqcO2nZZtU2OwQyIPyFZt24iHP3WfPF1dPs5usvn99e3sYp65XOVDZstCg3RYQM2d0hpdKUDmtpY5K5VOjXJ5oR2CAym4grqwWD2LquLciUqIfXKyzk23v40YB9M1cXqO7dGP0TApleRQaJlQtkZd8DEGrM0qNJ0NH4aBmTSbtWaTNJtJs5nij3_ix6rD578Tv14TwNdATKN-icG8-jH06cv_pH4Dm2eJiA</recordid><startdate>20141001</startdate><enddate>20141001</enddate><creator>Ji, Lili</creator><creator>Ni, Tingting</creator><creator>Shen, Yanbo</creator><creator>Xue, Qun</creator><creator>Liu, Yifei</creator><creator>Chen, Buyou</creator><creator>Cui, Xuefan</creator><creator>Lv, Liting</creator><creator>Yu, Xiafei</creator><creator>Cui, Yuan</creator><creator>Lu, Xiaoning</creator><creator>Chen, Jie</creator><creator>Mao, Guoxin</creator><creator>Wang, Yuchan</creator><general>Springer Netherlands</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></search><sort><creationdate>20141001</creationdate><title>Transformer 2β (Tra2β/SFRS10) positively regulates the progression of NSCLC via promoting cell proliferation</title><author>Ji, Lili ; Ni, Tingting ; Shen, Yanbo ; Xue, Qun ; Liu, Yifei ; Chen, Buyou ; Cui, Xuefan ; Lv, Liting ; Yu, Xiafei ; Cui, Yuan ; Lu, Xiaoning ; Chen, Jie ; Mao, Guoxin ; Wang, Yuchan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c484t-a76905ce60f2c899ec73054af5417894af8c469ce0c053280f6aebd3bb22c3b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Western</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Developmental Biology</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Life Sciences</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neoplasm Staging</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Original Paper</topic><topic>Prognosis</topic><topic>RNA Interference</topic><topic>RNA-Binding Proteins - genetics</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Serine-Arginine Splicing Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ji, Lili</creatorcontrib><creatorcontrib>Ni, Tingting</creatorcontrib><creatorcontrib>Shen, Yanbo</creatorcontrib><creatorcontrib>Xue, Qun</creatorcontrib><creatorcontrib>Liu, Yifei</creatorcontrib><creatorcontrib>Chen, Buyou</creatorcontrib><creatorcontrib>Cui, Xuefan</creatorcontrib><creatorcontrib>Lv, Liting</creatorcontrib><creatorcontrib>Yu, Xiafei</creatorcontrib><creatorcontrib>Cui, Yuan</creatorcontrib><creatorcontrib>Lu, Xiaoning</creatorcontrib><creatorcontrib>Chen, Jie</creatorcontrib><creatorcontrib>Mao, Guoxin</creatorcontrib><creatorcontrib>Wang, Yuchan</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>Journal of molecular histology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ji, Lili</au><au>Ni, Tingting</au><au>Shen, Yanbo</au><au>Xue, Qun</au><au>Liu, Yifei</au><au>Chen, Buyou</au><au>Cui, Xuefan</au><au>Lv, Liting</au><au>Yu, Xiafei</au><au>Cui, Yuan</au><au>Lu, Xiaoning</au><au>Chen, Jie</au><au>Mao, Guoxin</au><au>Wang, Yuchan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transformer 2β (Tra2β/SFRS10) positively regulates the progression of NSCLC via promoting cell proliferation</atitle><jtitle>Journal of molecular histology</jtitle><stitle>J Mol Hist</stitle><addtitle>J Mol Histol</addtitle><date>2014-10-01</date><risdate>2014</risdate><volume>45</volume><issue>5</issue><spage>573</spage><epage>582</epage><pages>573-582</pages><issn>1567-2379</issn><eissn>1567-2387</eissn><abstract>Transformer 2β (Tra2β), a member of the serine/arginine-rich-like protein family, is an important RNA-binding protein involved in alternative splice. Deregulation of Tra2β has been observed in several cancers. However, the detailed role of Tra2β in non-small cell lung cancer (NSCLC) has not been elucidated. In this study, the contribution of Tra2β to NSCLC development was investigated. On histological level, the expression of Tra2β was determined by Western and immunohistochemistry assays. It demonstrated that Tra2β was expressed higher in NSCLC tumor tissues compared with adjacent non-tumor tissues. In addition to confirm the association of Tra2β expression with histological differentiation and clinical stage (
p
< 0.05), we also confirmed significant positive correlation between the expression level of Tra2β and that of Ki67 (
p
< 0.05, r = 0.446) by Spearman rank correlation test. Moreover, high expression of Tra2β predicted poor prognosis by Kaplan–Meier survival analysis. And Tra2β among with other clinicopathologic variables was an independent prognostic indicator for patients’ overall survival by multivariate analysis. On cellular level, Tra2β expression was demonstrated to promote proliferation of NSCLC cells through a series of assays, including serum starvation and release assay, Western blot assay and flow cytometry analysis. Moreover, knockdown of Tra2β was confirmed to inhibit proliferation and to induce apoptosis of NSCLC cells through flow cytometry analysis, western analysis, cell counting kit-8 assay and Tunnel assay. Our results indicated that Tra2β was involved in the tumorigenesis of NSCLC and might be a potential therapeutic target of NSCLC.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>24952301</pmid><doi>10.1007/s10735-014-9582-3</doi><tpages>10</tpages></addata></record> |
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subjects | Biomedical and Life Sciences Biomedicine Blotting, Western Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Biology Cell Line, Tumor Cell Proliferation Developmental Biology Disease Progression Female Humans Immunohistochemistry Kaplan-Meier Estimate Ki-67 Antigen - metabolism Life Sciences Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Male Middle Aged Neoplasm Staging Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Original Paper Prognosis RNA Interference RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Serine-Arginine Splicing Factors |
title | Transformer 2β (Tra2β/SFRS10) positively regulates the progression of NSCLC via promoting cell proliferation |
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