PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma
Lung cancer is the leading cause of cancer-related mortality worldwide. PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of...
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| Veröffentlicht in: | Oncogenesis (New York, NY) NY), 2019-03, Vol.8 (3), p.22-22, Article 22 |
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| creator | Wang, Da-Yong Hong, Ya Chen, Ya-Ge Dong, Peng-Zhen Liu, Shi-Yu Gao, Ying-Ran Lu, Dan Li, Hui-Min Li, Tao Guo, Jian-Cheng He, Fei Ren, Xue-Qun Sun, Shi-Yong Wu, Dong-Dong Duan, Shao-Feng Ji, Xin-Ying |
| description | Lung cancer is the leading cause of cancer-related mortality worldwide. PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of PCNP in lung adenocarcinoma tissue was significantly higher than that in corresponding adjacent non-tumor tissue. Over-expression of PCNP promoted the proliferation, migration, and invasion of lung adenocarcinoma cells, while down-regulation of PCNP exhibited opposite effects. PCNP over-expression decreased apoptosis through up-regulating the expression levels of phospho (p)-signal transducers and activators of transcription (STAT) 3 and p-STAT5 in lung adenocarcinoma cells, whereas PCNP knockdown showed opposite trends. PCNP overexpression enhanced autophagy by increasing the expression levels of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) in lung adenocarcinoma cells, however an opposite trend was observed in the sh-PCNP group. In addition, overexpression of PCNP showed the tumor-promoting effect on xenografted lung adenocarcinoma, while PCNP knockdown reduced the growth of lung adenocarcinoma via regulating angiogenesis. Our study elucidates that PCNP can regulate the procession of human lung adenocarcinoma cells via STAT3/5 and PI3K/Akt/mTOR signaling pathways. PCNP may be considered as a promising biomarker for the diagnosis and prognosis in patients with lung adenocarcinoma. Furthermore, PCNP can be a novel therapeutic target and potent PCNP inhibitors can be designed and developed in the treatment of lung adenocarcinoma. |
| doi_str_mv | 10.1038/s41389-019-0132-4 |
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PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of PCNP in lung adenocarcinoma tissue was significantly higher than that in corresponding adjacent non-tumor tissue. Over-expression of PCNP promoted the proliferation, migration, and invasion of lung adenocarcinoma cells, while down-regulation of PCNP exhibited opposite effects. PCNP over-expression decreased apoptosis through up-regulating the expression levels of phospho (p)-signal transducers and activators of transcription (STAT) 3 and p-STAT5 in lung adenocarcinoma cells, whereas PCNP knockdown showed opposite trends. PCNP overexpression enhanced autophagy by increasing the expression levels of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) in lung adenocarcinoma cells, however an opposite trend was observed in the sh-PCNP group. In addition, overexpression of PCNP showed the tumor-promoting effect on xenografted lung adenocarcinoma, while PCNP knockdown reduced the growth of lung adenocarcinoma via regulating angiogenesis. Our study elucidates that PCNP can regulate the procession of human lung adenocarcinoma cells via STAT3/5 and PI3K/Akt/mTOR signaling pathways. PCNP may be considered as a promising biomarker for the diagnosis and prognosis in patients with lung adenocarcinoma. Furthermore, PCNP can be a novel therapeutic target and potent PCNP inhibitors can be designed and developed in the treatment of lung adenocarcinoma.</description><identifier>ISSN: 2157-9024</identifier><identifier>EISSN: 2157-9024</identifier><identifier>DOI: 10.1038/s41389-019-0132-4</identifier><identifier>PMID: 30872582</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; 13/1 ; 13/2 ; 13/89 ; 42/34 ; 631/67/1612 ; 631/80/83 ; 64/60 ; Adenocarcinoma ; AKT protein ; Angiogenesis ; Apoptosis ; Autophagy ; Cancer ; Cell Biology ; Cell migration ; Cell proliferation ; Human Genetics ; Internal Medicine ; Kinases ; Lung cancer ; Medicine ; Medicine & Public Health ; Oncology ; Overexpression ; Phagocytosis ; Rapamycin ; Stat3 protein ; Stat5 protein ; Therapeutic applications ; TOR protein ; Transcription factors ; Xenografts</subject><ispartof>Oncogenesis (New York, NY), 2019-03, Vol.8 (3), p.22-22, Article 22</ispartof><rights>The Author(s) 2019</rights><rights>This work is published under http://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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-3a47bc8f4272623d2827b3cda86b072f2fc4c8d3331af3e4067cb4741ae6e5953</citedby><cites>FETCH-LOGICAL-c470t-3a47bc8f4272623d2827b3cda86b072f2fc4c8d3331af3e4067cb4741ae6e5953</cites><orcidid>0000-0001-6739-8437</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6418141/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6418141/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30872582$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Da-Yong</creatorcontrib><creatorcontrib>Hong, Ya</creatorcontrib><creatorcontrib>Chen, Ya-Ge</creatorcontrib><creatorcontrib>Dong, Peng-Zhen</creatorcontrib><creatorcontrib>Liu, Shi-Yu</creatorcontrib><creatorcontrib>Gao, Ying-Ran</creatorcontrib><creatorcontrib>Lu, Dan</creatorcontrib><creatorcontrib>Li, Hui-Min</creatorcontrib><creatorcontrib>Li, Tao</creatorcontrib><creatorcontrib>Guo, Jian-Cheng</creatorcontrib><creatorcontrib>He, Fei</creatorcontrib><creatorcontrib>Ren, Xue-Qun</creatorcontrib><creatorcontrib>Sun, Shi-Yong</creatorcontrib><creatorcontrib>Wu, Dong-Dong</creatorcontrib><creatorcontrib>Duan, Shao-Feng</creatorcontrib><creatorcontrib>Ji, Xin-Ying</creatorcontrib><title>PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma</title><title>Oncogenesis (New York, NY)</title><addtitle>Oncogenesis</addtitle><addtitle>Oncogenesis</addtitle><description>Lung cancer is the leading cause of cancer-related mortality worldwide. PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of PCNP in lung adenocarcinoma tissue was significantly higher than that in corresponding adjacent non-tumor tissue. Over-expression of PCNP promoted the proliferation, migration, and invasion of lung adenocarcinoma cells, while down-regulation of PCNP exhibited opposite effects. PCNP over-expression decreased apoptosis through up-regulating the expression levels of phospho (p)-signal transducers and activators of transcription (STAT) 3 and p-STAT5 in lung adenocarcinoma cells, whereas PCNP knockdown showed opposite trends. PCNP overexpression enhanced autophagy by increasing the expression levels of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) in lung adenocarcinoma cells, however an opposite trend was observed in the sh-PCNP group. In addition, overexpression of PCNP showed the tumor-promoting effect on xenografted lung adenocarcinoma, while PCNP knockdown reduced the growth of lung adenocarcinoma via regulating angiogenesis. Our study elucidates that PCNP can regulate the procession of human lung adenocarcinoma cells via STAT3/5 and PI3K/Akt/mTOR signaling pathways. PCNP may be considered as a promising biomarker for the diagnosis and prognosis in patients with lung adenocarcinoma. Furthermore, PCNP can be a novel therapeutic target and potent PCNP inhibitors can be designed and developed in the treatment of lung adenocarcinoma.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>13/1</subject><subject>13/2</subject><subject>13/89</subject><subject>42/34</subject><subject>631/67/1612</subject><subject>631/80/83</subject><subject>64/60</subject><subject>Adenocarcinoma</subject><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Human Genetics</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Overexpression</subject><subject>Phagocytosis</subject><subject>Rapamycin</subject><subject>Stat3 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adenocarcinoma</title><author>Wang, Da-Yong ; Hong, Ya ; Chen, Ya-Ge ; Dong, Peng-Zhen ; Liu, Shi-Yu ; Gao, Ying-Ran ; Lu, Dan ; Li, Hui-Min ; Li, Tao ; Guo, Jian-Cheng ; He, Fei ; Ren, Xue-Qun ; Sun, Shi-Yong ; Wu, Dong-Dong ; Duan, Shao-Feng ; Ji, Xin-Ying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-3a47bc8f4272623d2827b3cda86b072f2fc4c8d3331af3e4067cb4741ae6e5953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>13/1</topic><topic>13/2</topic><topic>13/89</topic><topic>42/34</topic><topic>631/67/1612</topic><topic>631/80/83</topic><topic>64/60</topic><topic>Adenocarcinoma</topic><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Human 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Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogenesis (New York, NY)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Da-Yong</au><au>Hong, Ya</au><au>Chen, Ya-Ge</au><au>Dong, Peng-Zhen</au><au>Liu, Shi-Yu</au><au>Gao, Ying-Ran</au><au>Lu, Dan</au><au>Li, Hui-Min</au><au>Li, Tao</au><au>Guo, Jian-Cheng</au><au>He, Fei</au><au>Ren, Xue-Qun</au><au>Sun, Shi-Yong</au><au>Wu, Dong-Dong</au><au>Duan, Shao-Feng</au><au>Ji, Xin-Ying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma</atitle><jtitle>Oncogenesis (New York, NY)</jtitle><stitle>Oncogenesis</stitle><addtitle>Oncogenesis</addtitle><date>2019-03-14</date><risdate>2019</risdate><volume>8</volume><issue>3</issue><spage>22</spage><epage>22</epage><pages>22-22</pages><artnum>22</artnum><issn>2157-9024</issn><eissn>2157-9024</eissn><abstract>Lung cancer is the leading cause of cancer-related mortality worldwide. PEST-containing nuclear protein (PCNP) has been found in the nucleus of cancer cells. Whether PCNP plays a role in the growth of lung adenocarcinoma is still unknown. In the present study, the results indicated that the level of PCNP in lung adenocarcinoma tissue was significantly higher than that in corresponding adjacent non-tumor tissue. Over-expression of PCNP promoted the proliferation, migration, and invasion of lung adenocarcinoma cells, while down-regulation of PCNP exhibited opposite effects. PCNP over-expression decreased apoptosis through up-regulating the expression levels of phospho (p)-signal transducers and activators of transcription (STAT) 3 and p-STAT5 in lung adenocarcinoma cells, whereas PCNP knockdown showed opposite trends. PCNP overexpression enhanced autophagy by increasing the expression levels of p-phosphatidylinositol 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) in lung adenocarcinoma cells, however an opposite trend was observed in the sh-PCNP group. In addition, overexpression of PCNP showed the tumor-promoting effect on xenografted lung adenocarcinoma, while PCNP knockdown reduced the growth of lung adenocarcinoma via regulating angiogenesis. Our study elucidates that PCNP can regulate the procession of human lung adenocarcinoma cells via STAT3/5 and PI3K/Akt/mTOR signaling pathways. PCNP may be considered as a promising biomarker for the diagnosis and prognosis in patients with lung adenocarcinoma. Furthermore, PCNP can be a novel therapeutic target and potent PCNP inhibitors can be designed and developed in the treatment of lung adenocarcinoma.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30872582</pmid><doi>10.1038/s41389-019-0132-4</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-6739-8437</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase 13/1 13/2 13/89 42/34 631/67/1612 631/80/83 64/60 Adenocarcinoma AKT protein Angiogenesis Apoptosis Autophagy Cancer Cell Biology Cell migration Cell proliferation Human Genetics Internal Medicine Kinases Lung cancer Medicine Medicine & Public Health Oncology Overexpression Phagocytosis Rapamycin Stat3 protein Stat5 protein Therapeutic applications TOR protein Transcription factors Xenografts |
| title | PEST-containing nuclear protein regulates cell proliferation, migration, and invasion in lung adenocarcinoma |
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