Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression
Long non-coding RNAs (LncRNAs) have been suggested as important regulators of cancer development and progression in non-small cell lung cancer (NSCLC). Nevertheless, the biological roles and clinical significance of lncRNA UFC1 in NSCLC remain unclear. We detected the expression of UFC1 in tumor tis...
Gespeichert in:
| Veröffentlicht in: | Cell death & disease 2020-04, Vol.11 (4), p.215-215, Article 215 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 215 |
|---|---|
| container_issue | 4 |
| container_start_page | 215 |
| container_title | Cell death & disease |
| container_volume | 11 |
| creator | Zang, Xueyan Gu, Jianmei Zhang, Jiayin Shi, Hui Hou, Sinan Xu, Xueying Chen, Yanke Zhang, Yu Mao, Fei Qian, Hui Zhu, Taofeng Xu, Wenrong Zhang, Xu |
| description | Long non-coding RNAs (LncRNAs) have been suggested as important regulators of cancer development and progression in non-small cell lung cancer (NSCLC). Nevertheless, the biological roles and clinical significance of lncRNA UFC1 in NSCLC remain unclear. We detected the expression of UFC1 in tumor tissues, serum, and serum exosomes of NSCLC patients by qRT-PCR. Gene overexpression or silencing were used to examine the biological roles of UFC1 in NSCLC. RNA immunoprecipitation and ChIP assays were performed to evaluate the interaction between UFC1 and enhancer of zeste homolog 2 (EZH2) and the binding of EZH2 to PTEN gene promoter. Rescue study was used to access the importance of PTEN regulation by UFC1 in NSCLC progression. UFC1 expression was upregulated in tumor tissues, serum, and serum exosomes of NSCLC patients and high level of UFC1 was associated with tumor infiltration. UFC1 knockdown inhibited NSCLC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. UFC1 overexpression led to the opposite effects. Mechanistically, UFC1 bound to EZH2 and mediated its accumulation at the promoter region of PTEN gene, resulting in the trimethylation of H3K27 and the inhibition of PTEN expression. UFC1 knockdown inhibited NSCLC growth in mouse xenograft tumor models while the simultaneous depletion of PTEN reversed this effect. NSCLC cells derived exosomes could promote NSCLC cell proliferation, migration and invasion through the transfer of UFC1. Moreover, Exosome-transmitted UFC1 promotes NSCLC progression by inhibiting PTEN expression via EZH2-mediated epigenetic silencing. Exosome-mediated transmit of UFC1 may represent a new mechanism for NSCLC progression and provide a potential marker for NSCLC diagnosis. |
| doi_str_mv | 10.1038/s41419-020-2409-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7118073</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2386274130</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-c681bfb89809202265b716ecc25561fae63b4259327bc7e16cf620b7026a017d3</originalsourceid><addsrcrecordid>eNp1kcFu1DAQhiMEolXpA3BBlrhwcbHHiZ1ckKrVliJVBaH2wsVyvJPgKrEXO6naN-Cx67BLKUj44rHmm39m_BfFa85OOBP1-1TykjeUAaNQshw8Kw6BlZyWdd08fxIfFMcp3bB8hGBQyZfFgQAoIb8Pi5_ru5DCiHSKxqfRTRNuyODt18tTcn224mQbwxgmTMQHT9NohoFaHAYyzL4n1niLcWH6iCm54El7T9bfzoGOuHFmEcOt69Hj5CxJbkBvXS4MHflytb4keLfdF74qXnRmSHi8v4-K67P11eqcXnz--Gl1ekFtqdhErax527V1U7MGGICsWsUlWgtVJXlnUIq2hKoRoFqrkEvbSWCtYiAN42ojjooPO93t3OYZLfq8-aC30Y0m3utgnP4749133YdbrTivmRJZ4N1eIIYfM6ZJjy4tX2I8hjlpELUEVXLBMvr2H_QmzNHn9X5RQlWCNZniO8rGkFLE7nEYzvRitd5ZrbPVerFaL8pvnm7xWPHb2AzADkg55XuMf1r_X_UBNmO0rA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2386375309</pqid></control><display><type>article</type><title>Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Springer Nature OA Free Journals</source><source>Nature Free</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Zang, Xueyan ; Gu, Jianmei ; Zhang, Jiayin ; Shi, Hui ; Hou, Sinan ; Xu, Xueying ; Chen, Yanke ; Zhang, Yu ; Mao, Fei ; Qian, Hui ; Zhu, Taofeng ; Xu, Wenrong ; Zhang, Xu</creator><creatorcontrib>Zang, Xueyan ; Gu, Jianmei ; Zhang, Jiayin ; Shi, Hui ; Hou, Sinan ; Xu, Xueying ; Chen, Yanke ; Zhang, Yu ; Mao, Fei ; Qian, Hui ; Zhu, Taofeng ; Xu, Wenrong ; Zhang, Xu</creatorcontrib><description>Long non-coding RNAs (LncRNAs) have been suggested as important regulators of cancer development and progression in non-small cell lung cancer (NSCLC). Nevertheless, the biological roles and clinical significance of lncRNA UFC1 in NSCLC remain unclear. We detected the expression of UFC1 in tumor tissues, serum, and serum exosomes of NSCLC patients by qRT-PCR. Gene overexpression or silencing were used to examine the biological roles of UFC1 in NSCLC. RNA immunoprecipitation and ChIP assays were performed to evaluate the interaction between UFC1 and enhancer of zeste homolog 2 (EZH2) and the binding of EZH2 to PTEN gene promoter. Rescue study was used to access the importance of PTEN regulation by UFC1 in NSCLC progression. UFC1 expression was upregulated in tumor tissues, serum, and serum exosomes of NSCLC patients and high level of UFC1 was associated with tumor infiltration. UFC1 knockdown inhibited NSCLC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. UFC1 overexpression led to the opposite effects. Mechanistically, UFC1 bound to EZH2 and mediated its accumulation at the promoter region of PTEN gene, resulting in the trimethylation of H3K27 and the inhibition of PTEN expression. UFC1 knockdown inhibited NSCLC growth in mouse xenograft tumor models while the simultaneous depletion of PTEN reversed this effect. NSCLC cells derived exosomes could promote NSCLC cell proliferation, migration and invasion through the transfer of UFC1. Moreover, Exosome-transmitted UFC1 promotes NSCLC progression by inhibiting PTEN expression via EZH2-mediated epigenetic silencing. Exosome-mediated transmit of UFC1 may represent a new mechanism for NSCLC progression and provide a potential marker for NSCLC diagnosis.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2409-0</identifier><identifier>PMID: 32242003</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 38/77 ; 38/89 ; 631/67/1612/1350 ; 692/308/53/2421 ; A549 Cells ; Animal models ; Animals ; Antibodies ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Case-Control Studies ; Cell Biology ; Cell Culture ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement - physiology ; Cell proliferation ; Cell Proliferation - physiology ; Disease Models, Animal ; Disease Progression ; Enhancer of Zeste Homolog 2 Protein - genetics ; Enhancer of Zeste Homolog 2 Protein - metabolism ; Epigenesis, Genetic ; Epigenetics ; Exosomes ; Exosomes - genetics ; Exosomes - metabolism ; Exosomes - pathology ; Heterografts ; Humans ; Immunology ; Immunoprecipitation ; Life Sciences ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Male ; Metastases ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Invasiveness ; Non-coding RNA ; Non-small cell lung carcinoma ; PTEN Phosphohydrolase - biosynthesis ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; PTEN protein ; Ribonucleic acid ; RNA ; RNA, Long Noncoding ; Small cell lung carcinoma ; Transfection ; Ubiquitin-Conjugating Enzymes - genetics ; Ubiquitin-Conjugating Enzymes - metabolism ; Up-Regulation ; Xenografts</subject><ispartof>Cell death & disease, 2020-04, Vol.11 (4), p.215-215, Article 215</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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-c681bfb89809202265b716ecc25561fae63b4259327bc7e16cf620b7026a017d3</citedby><cites>FETCH-LOGICAL-c470t-c681bfb89809202265b716ecc25561fae63b4259327bc7e16cf620b7026a017d3</cites><orcidid>0000-0001-5840-4436</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/PMC7118073/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7118073/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,41119,42188,51575,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32242003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zang, Xueyan</creatorcontrib><creatorcontrib>Gu, Jianmei</creatorcontrib><creatorcontrib>Zhang, Jiayin</creatorcontrib><creatorcontrib>Shi, Hui</creatorcontrib><creatorcontrib>Hou, Sinan</creatorcontrib><creatorcontrib>Xu, Xueying</creatorcontrib><creatorcontrib>Chen, Yanke</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Mao, Fei</creatorcontrib><creatorcontrib>Qian, Hui</creatorcontrib><creatorcontrib>Zhu, Taofeng</creatorcontrib><creatorcontrib>Xu, Wenrong</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><title>Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Long non-coding RNAs (LncRNAs) have been suggested as important regulators of cancer development and progression in non-small cell lung cancer (NSCLC). Nevertheless, the biological roles and clinical significance of lncRNA UFC1 in NSCLC remain unclear. We detected the expression of UFC1 in tumor tissues, serum, and serum exosomes of NSCLC patients by qRT-PCR. Gene overexpression or silencing were used to examine the biological roles of UFC1 in NSCLC. RNA immunoprecipitation and ChIP assays were performed to evaluate the interaction between UFC1 and enhancer of zeste homolog 2 (EZH2) and the binding of EZH2 to PTEN gene promoter. Rescue study was used to access the importance of PTEN regulation by UFC1 in NSCLC progression. UFC1 expression was upregulated in tumor tissues, serum, and serum exosomes of NSCLC patients and high level of UFC1 was associated with tumor infiltration. UFC1 knockdown inhibited NSCLC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. UFC1 overexpression led to the opposite effects. Mechanistically, UFC1 bound to EZH2 and mediated its accumulation at the promoter region of PTEN gene, resulting in the trimethylation of H3K27 and the inhibition of PTEN expression. UFC1 knockdown inhibited NSCLC growth in mouse xenograft tumor models while the simultaneous depletion of PTEN reversed this effect. NSCLC cells derived exosomes could promote NSCLC cell proliferation, migration and invasion through the transfer of UFC1. Moreover, Exosome-transmitted UFC1 promotes NSCLC progression by inhibiting PTEN expression via EZH2-mediated epigenetic silencing. Exosome-mediated transmit of UFC1 may represent a new mechanism for NSCLC progression and provide a potential marker for NSCLC diagnosis.</description><subject>13/109</subject><subject>38/77</subject><subject>38/89</subject><subject>631/67/1612/1350</subject><subject>692/308/53/2421</subject><subject>A549 Cells</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</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>Case-Control Studies</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - physiology</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - physiology</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Enhancer of Zeste Homolog 2 Protein - genetics</subject><subject>Enhancer of Zeste Homolog 2 Protein - metabolism</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Exosomes</subject><subject>Exosomes - genetics</subject><subject>Exosomes - metabolism</subject><subject>Exosomes - pathology</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Immunology</subject><subject>Immunoprecipitation</subject><subject>Life Sciences</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Neoplasm Invasiveness</subject><subject>Non-coding RNA</subject><subject>Non-small cell lung carcinoma</subject><subject>PTEN Phosphohydrolase - biosynthesis</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>PTEN protein</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding</subject><subject>Small cell lung carcinoma</subject><subject>Transfection</subject><subject>Ubiquitin-Conjugating Enzymes - genetics</subject><subject>Ubiquitin-Conjugating Enzymes - metabolism</subject><subject>Up-Regulation</subject><subject>Xenografts</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kcFu1DAQhiMEolXpA3BBlrhwcbHHiZ1ckKrVliJVBaH2wsVyvJPgKrEXO6naN-Cx67BLKUj44rHmm39m_BfFa85OOBP1-1TykjeUAaNQshw8Kw6BlZyWdd08fxIfFMcp3bB8hGBQyZfFgQAoIb8Pi5_ru5DCiHSKxqfRTRNuyODt18tTcn224mQbwxgmTMQHT9NohoFaHAYyzL4n1niLcWH6iCm54El7T9bfzoGOuHFmEcOt69Hj5CxJbkBvXS4MHflytb4keLfdF74qXnRmSHi8v4-K67P11eqcXnz--Gl1ekFtqdhErax527V1U7MGGICsWsUlWgtVJXlnUIq2hKoRoFqrkEvbSWCtYiAN42ojjooPO93t3OYZLfq8-aC30Y0m3utgnP4749133YdbrTivmRJZ4N1eIIYfM6ZJjy4tX2I8hjlpELUEVXLBMvr2H_QmzNHn9X5RQlWCNZniO8rGkFLE7nEYzvRitd5ZrbPVerFaL8pvnm7xWPHb2AzADkg55XuMf1r_X_UBNmO0rA</recordid><startdate>20200402</startdate><enddate>20200402</enddate><creator>Zang, Xueyan</creator><creator>Gu, Jianmei</creator><creator>Zhang, Jiayin</creator><creator>Shi, Hui</creator><creator>Hou, Sinan</creator><creator>Xu, Xueying</creator><creator>Chen, Yanke</creator><creator>Zhang, Yu</creator><creator>Mao, Fei</creator><creator>Qian, Hui</creator><creator>Zhu, Taofeng</creator><creator>Xu, Wenrong</creator><creator>Zhang, Xu</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><scope>C6C</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5840-4436</orcidid></search><sort><creationdate>20200402</creationdate><title>Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression</title><author>Zang, Xueyan ; Gu, Jianmei ; Zhang, Jiayin ; Shi, Hui ; Hou, Sinan ; Xu, Xueying ; Chen, Yanke ; Zhang, Yu ; Mao, Fei ; Qian, Hui ; Zhu, Taofeng ; Xu, Wenrong ; Zhang, Xu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-c681bfb89809202265b716ecc25561fae63b4259327bc7e16cf620b7026a017d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/109</topic><topic>38/77</topic><topic>38/89</topic><topic>631/67/1612/1350</topic><topic>692/308/53/2421</topic><topic>A549 Cells</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</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>Case-Control Studies</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - physiology</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - physiology</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Enhancer of Zeste Homolog 2 Protein - genetics</topic><topic>Enhancer of Zeste Homolog 2 Protein - metabolism</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Exosomes</topic><topic>Exosomes - genetics</topic><topic>Exosomes - metabolism</topic><topic>Exosomes - pathology</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Immunology</topic><topic>Immunoprecipitation</topic><topic>Life Sciences</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Neoplasm Invasiveness</topic><topic>Non-coding RNA</topic><topic>Non-small cell lung carcinoma</topic><topic>PTEN Phosphohydrolase - biosynthesis</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>PTEN protein</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding</topic><topic>Small cell lung carcinoma</topic><topic>Transfection</topic><topic>Ubiquitin-Conjugating Enzymes - genetics</topic><topic>Ubiquitin-Conjugating Enzymes - metabolism</topic><topic>Up-Regulation</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zang, Xueyan</creatorcontrib><creatorcontrib>Gu, Jianmei</creatorcontrib><creatorcontrib>Zhang, Jiayin</creatorcontrib><creatorcontrib>Shi, Hui</creatorcontrib><creatorcontrib>Hou, Sinan</creatorcontrib><creatorcontrib>Xu, Xueying</creatorcontrib><creatorcontrib>Chen, Yanke</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Mao, Fei</creatorcontrib><creatorcontrib>Qian, Hui</creatorcontrib><creatorcontrib>Zhu, Taofeng</creatorcontrib><creatorcontrib>Xu, Wenrong</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zang, Xueyan</au><au>Gu, Jianmei</au><au>Zhang, Jiayin</au><au>Shi, Hui</au><au>Hou, Sinan</au><au>Xu, Xueying</au><au>Chen, Yanke</au><au>Zhang, Yu</au><au>Mao, Fei</au><au>Qian, Hui</au><au>Zhu, Taofeng</au><au>Xu, Wenrong</au><au>Zhang, Xu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-04-02</date><risdate>2020</risdate><volume>11</volume><issue>4</issue><spage>215</spage><epage>215</epage><pages>215-215</pages><artnum>215</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Long non-coding RNAs (LncRNAs) have been suggested as important regulators of cancer development and progression in non-small cell lung cancer (NSCLC). Nevertheless, the biological roles and clinical significance of lncRNA UFC1 in NSCLC remain unclear. We detected the expression of UFC1 in tumor tissues, serum, and serum exosomes of NSCLC patients by qRT-PCR. Gene overexpression or silencing were used to examine the biological roles of UFC1 in NSCLC. RNA immunoprecipitation and ChIP assays were performed to evaluate the interaction between UFC1 and enhancer of zeste homolog 2 (EZH2) and the binding of EZH2 to PTEN gene promoter. Rescue study was used to access the importance of PTEN regulation by UFC1 in NSCLC progression. UFC1 expression was upregulated in tumor tissues, serum, and serum exosomes of NSCLC patients and high level of UFC1 was associated with tumor infiltration. UFC1 knockdown inhibited NSCLC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. UFC1 overexpression led to the opposite effects. Mechanistically, UFC1 bound to EZH2 and mediated its accumulation at the promoter region of PTEN gene, resulting in the trimethylation of H3K27 and the inhibition of PTEN expression. UFC1 knockdown inhibited NSCLC growth in mouse xenograft tumor models while the simultaneous depletion of PTEN reversed this effect. NSCLC cells derived exosomes could promote NSCLC cell proliferation, migration and invasion through the transfer of UFC1. Moreover, Exosome-transmitted UFC1 promotes NSCLC progression by inhibiting PTEN expression via EZH2-mediated epigenetic silencing. Exosome-mediated transmit of UFC1 may represent a new mechanism for NSCLC progression and provide a potential marker for NSCLC diagnosis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32242003</pmid><doi>10.1038/s41419-020-2409-0</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-5840-4436</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2041-4889 |
| ispartof | Cell death & disease, 2020-04, Vol.11 (4), p.215-215, Article 215 |
| issn | 2041-4889 2041-4889 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7118073 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | 13/109 38/77 38/89 631/67/1612/1350 692/308/53/2421 A549 Cells Animal models Animals Antibodies Apoptosis Biochemistry Biomedical and Life Sciences Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Case-Control Studies Cell Biology Cell Culture Cell cycle Cell growth Cell Line, Tumor Cell migration Cell Movement - physiology Cell proliferation Cell Proliferation - physiology Disease Models, Animal Disease Progression Enhancer of Zeste Homolog 2 Protein - genetics Enhancer of Zeste Homolog 2 Protein - metabolism Epigenesis, Genetic Epigenetics Exosomes Exosomes - genetics Exosomes - metabolism Exosomes - pathology Heterografts Humans Immunology Immunoprecipitation Life Sciences Lung cancer Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Male Metastases Mice Mice, Inbred BALB C Mice, Nude Neoplasm Invasiveness Non-coding RNA Non-small cell lung carcinoma PTEN Phosphohydrolase - biosynthesis PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism PTEN protein Ribonucleic acid RNA RNA, Long Noncoding Small cell lung carcinoma Transfection Ubiquitin-Conjugating Enzymes - genetics Ubiquitin-Conjugating Enzymes - metabolism Up-Regulation Xenografts |
| title | Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-10T11%3A35%3A18IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Exosome-transmitted%20lncRNA%20UFC1%20promotes%20non-small-cell%20lung%20cancer%20progression%20by%20EZH2-mediated%20epigenetic%20silencing%20of%20PTEN%20expression&rft.jtitle=Cell%20death%20&%20disease&rft.au=Zang,%20Xueyan&rft.date=2020-04-02&rft.volume=11&rft.issue=4&rft.spage=215&rft.epage=215&rft.pages=215-215&rft.artnum=215&rft.issn=2041-4889&rft.eissn=2041-4889&rft_id=info:doi/10.1038/s41419-020-2409-0&rft_dat=%3Cproquest_pubme%3E2386274130%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2386375309&rft_id=info:pmid/32242003&rfr_iscdi=true |