Expression and clinical role of NF45 as a novel cell cycle protein in esophageal squamous cell carcinoma (ESCC)
NF45 (also known as ILF2), as one subunit of NF-AT (nuclear factor of activated T cells), repairs DNA breaks, inhibits viral replication, and also functions as a negative regulator in the microRNA processing pathway in combination with NF90. Recently, it was found that implicated in the mitotic cont...
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| Veröffentlicht in: | Tumor biology 2015-02, Vol.36 (2), p.747-756 |
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| description | NF45 (also known as ILF2), as one subunit of NF-AT (nuclear factor of activated T cells), repairs DNA breaks, inhibits viral replication, and also functions as a negative regulator in the microRNA processing pathway in combination with NF90. Recently, it was found that implicated in the mitotic control of HeLa cells and deletion of endogenous NF45 decreases growth of HeLa cells. While the role of NF45 in cancer biology remains under debate. In this study, we analyzed the expression and clinical significance of NF45 in esophageal squamous cell carcinoma ESCC. The expression of NF45 was evaluated by Western blot in 8 paired fresh ESCC tissues and immunohistochemistry on 105 paraffin-embedded slices. NF45 was highly expressed in ESCC and significantly associated with ESCC cells tumor stage and Ki-67. Besides, high NF45 expression was an independent prognostic factor for ESCC patients’ poor survival. To determine whether NF45 could regulate the proliferation of ESCC cells, we increased endogenous NF45 and analyzed the proliferation of TE1 ESCC cells using Western blot, CCK8, flow cytometry assays and colony formation analyses, which together indicated that overexpression of NF45 favors cell cycle progress of TE1 ESCC cells. While knockdown of NF45 resulted in cell cycle arrest at G0/G1-phase and thus abolished the cell growth. These findings suggested that NF45 might play an important role in promoting the tumorigenesis of ESCC, and thus be a promising therapeutic target to prevent ESCC progression. |
| doi_str_mv | 10.1007/s13277-014-2683-5 |
| format | Article |
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Recently, it was found that implicated in the mitotic control of HeLa cells and deletion of endogenous NF45 decreases growth of HeLa cells. While the role of NF45 in cancer biology remains under debate. In this study, we analyzed the expression and clinical significance of NF45 in esophageal squamous cell carcinoma ESCC. The expression of NF45 was evaluated by Western blot in 8 paired fresh ESCC tissues and immunohistochemistry on 105 paraffin-embedded slices. NF45 was highly expressed in ESCC and significantly associated with ESCC cells tumor stage and Ki-67. Besides, high NF45 expression was an independent prognostic factor for ESCC patients’ poor survival. To determine whether NF45 could regulate the proliferation of ESCC cells, we increased endogenous NF45 and analyzed the proliferation of TE1 ESCC cells using Western blot, CCK8, flow cytometry assays and colony formation analyses, which together indicated that overexpression of NF45 favors cell cycle progress of TE1 ESCC cells. While knockdown of NF45 resulted in cell cycle arrest at G0/G1-phase and thus abolished the cell growth. These findings suggested that NF45 might play an important role in promoting the tumorigenesis of ESCC, and thus be a promising therapeutic target to prevent ESCC progression.</description><identifier>ISSN: 1010-4283</identifier><identifier>EISSN: 1423-0380</identifier><identifier>DOI: 10.1007/s13277-014-2683-5</identifier><identifier>PMID: 25286760</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Apoptosis - genetics ; Biomarkers, Tumor - biosynthesis ; Biomarkers, Tumor - genetics ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Carcinogenesis ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell cycle ; Cell Proliferation - genetics ; Esophageal cancer ; Esophageal Neoplasms - drug therapy ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Esophageal Squamous Cell Carcinoma ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HeLa Cells ; Humans ; Nuclear Factor 45 Protein - biosynthesis ; Nuclear Factor 45 Protein - genetics ; Prognosis ; Proteins ; Research Article</subject><ispartof>Tumor biology, 2015-02, Vol.36 (2), p.747-756</ispartof><rights>International Society of Oncology and BioMarkers (ISOBM) 2014</rights><rights>International Society of Oncology and BioMarkers (ISOBM) 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-764d4bdf4b2eecc9159b35d875768e6ffe350b7651eeae0874422665a18f83753</citedby><cites>FETCH-LOGICAL-c508t-764d4bdf4b2eecc9159b35d875768e6ffe350b7651eeae0874422665a18f83753</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/s13277-014-2683-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13277-014-2683-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,782,786,27931,27932,41495,42564,51326</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25286760$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ni, Sujie</creatorcontrib><creatorcontrib>Zhu, Junya</creatorcontrib><creatorcontrib>Zhang, Jianguo</creatorcontrib><creatorcontrib>Zhang, Shu</creatorcontrib><creatorcontrib>Li, Mei</creatorcontrib><creatorcontrib>Ni, Runzhou</creatorcontrib><creatorcontrib>Liu, Jinxia</creatorcontrib><creatorcontrib>Qiu, Huiyuan</creatorcontrib><creatorcontrib>Chen, Wenjuan</creatorcontrib><creatorcontrib>Wang, Huijie</creatorcontrib><creatorcontrib>Guo, Weijian</creatorcontrib><title>Expression and clinical role of NF45 as a novel cell cycle protein in esophageal squamous cell carcinoma (ESCC)</title><title>Tumor biology</title><addtitle>Tumor Biol</addtitle><addtitle>Tumour Biol</addtitle><description>NF45 (also known as ILF2), as one subunit of NF-AT (nuclear factor of activated T cells), repairs DNA breaks, inhibits viral replication, and also functions as a negative regulator in the microRNA processing pathway in combination with NF90. Recently, it was found that implicated in the mitotic control of HeLa cells and deletion of endogenous NF45 decreases growth of HeLa cells. While the role of NF45 in cancer biology remains under debate. In this study, we analyzed the expression and clinical significance of NF45 in esophageal squamous cell carcinoma ESCC. The expression of NF45 was evaluated by Western blot in 8 paired fresh ESCC tissues and immunohistochemistry on 105 paraffin-embedded slices. NF45 was highly expressed in ESCC and significantly associated with ESCC cells tumor stage and Ki-67. Besides, high NF45 expression was an independent prognostic factor for ESCC patients’ poor survival. To determine whether NF45 could regulate the proliferation of ESCC cells, we increased endogenous NF45 and analyzed the proliferation of TE1 ESCC cells using Western blot, CCK8, flow cytometry assays and colony formation analyses, which together indicated that overexpression of NF45 favors cell cycle progress of TE1 ESCC cells. While knockdown of NF45 resulted in cell cycle arrest at G0/G1-phase and thus abolished the cell growth. These findings suggested that NF45 might play an important role in promoting the tumorigenesis of ESCC, and thus be a promising therapeutic target to prevent ESCC progression.</description><subject>Apoptosis - genetics</subject><subject>Biomarkers, Tumor - biosynthesis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinogenesis</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell cycle</subject><subject>Cell Proliferation - genetics</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - drug therapy</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophageal Squamous Cell Carcinoma</subject><subject>Gene 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Runzhou</au><au>Liu, Jinxia</au><au>Qiu, Huiyuan</au><au>Chen, Wenjuan</au><au>Wang, Huijie</au><au>Guo, Weijian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression and clinical role of NF45 as a novel cell cycle protein in esophageal squamous cell carcinoma (ESCC)</atitle><jtitle>Tumor biology</jtitle><stitle>Tumor Biol</stitle><addtitle>Tumour Biol</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>36</volume><issue>2</issue><spage>747</spage><epage>756</epage><pages>747-756</pages><issn>1010-4283</issn><eissn>1423-0380</eissn><abstract>NF45 (also known as ILF2), as one subunit of NF-AT (nuclear factor of activated T cells), repairs DNA breaks, inhibits viral replication, and also functions as a negative regulator in the microRNA processing pathway in combination with NF90. Recently, it was found that implicated in the mitotic control of HeLa cells and deletion of endogenous NF45 decreases growth of HeLa cells. While the role of NF45 in cancer biology remains under debate. In this study, we analyzed the expression and clinical significance of NF45 in esophageal squamous cell carcinoma ESCC. The expression of NF45 was evaluated by Western blot in 8 paired fresh ESCC tissues and immunohistochemistry on 105 paraffin-embedded slices. NF45 was highly expressed in ESCC and significantly associated with ESCC cells tumor stage and Ki-67. Besides, high NF45 expression was an independent prognostic factor for ESCC patients’ poor survival. To determine whether NF45 could regulate the proliferation of ESCC cells, we increased endogenous NF45 and analyzed the proliferation of TE1 ESCC cells using Western blot, CCK8, flow cytometry assays and colony formation analyses, which together indicated that overexpression of NF45 favors cell cycle progress of TE1 ESCC cells. While knockdown of NF45 resulted in cell cycle arrest at G0/G1-phase and thus abolished the cell growth. These findings suggested that NF45 might play an important role in promoting the tumorigenesis of ESCC, and thus be a promising therapeutic target to prevent ESCC progression.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>25286760</pmid><doi>10.1007/s13277-014-2683-5</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis - genetics Biomarkers, Tumor - biosynthesis Biomarkers, Tumor - genetics Biomedical and Life Sciences Biomedicine Cancer Research Carcinogenesis Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell cycle Cell Proliferation - genetics Esophageal cancer Esophageal Neoplasms - drug therapy Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology Esophageal Squamous Cell Carcinoma Gene expression Gene Expression Regulation, Neoplastic Gene Knockdown Techniques HeLa Cells Humans Nuclear Factor 45 Protein - biosynthesis Nuclear Factor 45 Protein - genetics Prognosis Proteins Research Article |
| title | Expression and clinical role of NF45 as a novel cell cycle protein in esophageal squamous cell carcinoma (ESCC) |
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