Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells

Long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is abnormally expressed in numerous tumors and functions as an oncogene, but the role of NEAT1 in laryngocarcinoma is largely unknown. Our study validated that NEAT1 expression was markedly upregulated in laryngocarcinoma ti...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Aging (Albany, NY.) NY.), 2021-11, Vol.13 (22), p.24850-24865
Hauptverfasser: Zhang, Jiajia, Wang, Ping, Cui, Yanli
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 24865
container_issue 22
container_start_page 24850
container_title Aging (Albany, NY.)
container_volume 13
creator Zhang, Jiajia
Wang, Ping
Cui, Yanli
description Long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is abnormally expressed in numerous tumors and functions as an oncogene, but the role of NEAT1 in laryngocarcinoma is largely unknown. Our study validated that NEAT1 expression was markedly upregulated in laryngocarcinoma tissues and cells. Downregulation of NEAT1 dramatically suppressed cell proliferation and invasion through inhibiting miR-524-5p expression. Additionally, NEAT1 overexpression promoted cell growth and metastasis, while overexpression of miR-524-5p could reverse the effect. NEAT1 increased the expression of histone deacetylase 1 gene (HDAC1) via sponging miR-524-5p. Mechanistically, overexpression of HDAC1 recovered the cancer-inhibiting effects of miR-524-5p mimic or NEAT1 silence by deacetylation of tensin homolog deleted on chromosome ten (PTEN) and inhibiting AKT signal pathway. Moreover, experiments indicated that silence of NEAT1 signally suppressed tumor growth. Taken together, knockdown of NEAT1 suppressed laryngocarcinoma cell growth and metastasis by miR-524-5p/HDAC1/PTEN/AKT signal pathway, which provided a potential therapeutic target for laryngocarcinoma.
doi_str_mv 10.18632/aging.203719
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8660614</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2604018371</sourcerecordid><originalsourceid>FETCH-LOGICAL-c387t-92cd437a60266b89bdcf34d659527b9f36042ecf981bd12beed6f320206214003</originalsourceid><addsrcrecordid>eNpVkUtP4zAUhS00iEdhyXbk5WwCfsVxNkhVpzykqiBU1pbjOKlHiV3sFA3_hp-KaQsqK1_5Hn_3XB8ALjC6xIJTcqVa69pLgmiBywNwgkuWZywX5a-9-hicxvgPIZ7njB-BY8oELYQoTsD7zLsWOu-0rxMHPs3HcD4dLzC0bmkrO0Q4LA1U2gxvnRqsd9A38HExnaf74NftctPv7VOWE5blK3h193c8wVD9t-mph6vgez-YjSrVnW1M2HKUq9OQVxV30E6FN9ca1UGtnDYBatN18QwcNqqL5nx3jsDzzXQxuctmD7f3k_Es01QUQ1YSXTNaKI4I55Uoq1o3lNU8L3NSVGVDOWLE6KYUuKoxqYypeUMJIogTzBCiI3C95a7WVW9qbdwQVCdXwfbJl_TKyp8dZ5ey9a9ScI44ZgnwZwcI_mVt4iB7Gz9XUM74dZQkOUA4_TtO0mwr1cHHGEzzPQYjuUlVblKV21ST_ve-t2_1V4z0A1mkn1g</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2604018371</pqid></control><display><type>article</type><title>Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>PubMed Central</source><creator>Zhang, Jiajia ; Wang, Ping ; Cui, Yanli</creator><creatorcontrib>Zhang, Jiajia ; Wang, Ping ; Cui, Yanli</creatorcontrib><description>Long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is abnormally expressed in numerous tumors and functions as an oncogene, but the role of NEAT1 in laryngocarcinoma is largely unknown. Our study validated that NEAT1 expression was markedly upregulated in laryngocarcinoma tissues and cells. Downregulation of NEAT1 dramatically suppressed cell proliferation and invasion through inhibiting miR-524-5p expression. Additionally, NEAT1 overexpression promoted cell growth and metastasis, while overexpression of miR-524-5p could reverse the effect. NEAT1 increased the expression of histone deacetylase 1 gene (HDAC1) via sponging miR-524-5p. Mechanistically, overexpression of HDAC1 recovered the cancer-inhibiting effects of miR-524-5p mimic or NEAT1 silence by deacetylation of tensin homolog deleted on chromosome ten (PTEN) and inhibiting AKT signal pathway. Moreover, experiments indicated that silence of NEAT1 signally suppressed tumor growth. Taken together, knockdown of NEAT1 suppressed laryngocarcinoma cell growth and metastasis by miR-524-5p/HDAC1/PTEN/AKT signal pathway, which provided a potential therapeutic target for laryngocarcinoma.</description><identifier>ISSN: 1945-4589</identifier><identifier>EISSN: 1945-4589</identifier><identifier>DOI: 10.18632/aging.203719</identifier><identifier>PMID: 34837887</identifier><language>eng</language><publisher>United States: Impact Journals</publisher><subject>Acetylation ; Adult ; Cell Proliferation - genetics ; Female ; Histone Deacetylase 1 - genetics ; Histone Deacetylase 1 - metabolism ; Humans ; Laryngeal Neoplasms - genetics ; Laryngeal Neoplasms - metabolism ; Laryngeal Neoplasms - pathology ; Male ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; Neoplasm Invasiveness - genetics ; PTEN Phosphohydrolase - chemistry ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; Research Paper ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism</subject><ispartof>Aging (Albany, NY.), 2021-11, Vol.13 (22), p.24850-24865</ispartof><rights>Copyright: © 2021 Zhang et al.</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-92cd437a60266b89bdcf34d659527b9f36042ecf981bd12beed6f320206214003</citedby><cites>FETCH-LOGICAL-c387t-92cd437a60266b89bdcf34d659527b9f36042ecf981bd12beed6f320206214003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8660614/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8660614/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34837887$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Jiajia</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><creatorcontrib>Cui, Yanli</creatorcontrib><title>Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells</title><title>Aging (Albany, NY.)</title><addtitle>Aging (Albany NY)</addtitle><description>Long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is abnormally expressed in numerous tumors and functions as an oncogene, but the role of NEAT1 in laryngocarcinoma is largely unknown. Our study validated that NEAT1 expression was markedly upregulated in laryngocarcinoma tissues and cells. Downregulation of NEAT1 dramatically suppressed cell proliferation and invasion through inhibiting miR-524-5p expression. Additionally, NEAT1 overexpression promoted cell growth and metastasis, while overexpression of miR-524-5p could reverse the effect. NEAT1 increased the expression of histone deacetylase 1 gene (HDAC1) via sponging miR-524-5p. Mechanistically, overexpression of HDAC1 recovered the cancer-inhibiting effects of miR-524-5p mimic or NEAT1 silence by deacetylation of tensin homolog deleted on chromosome ten (PTEN) and inhibiting AKT signal pathway. Moreover, experiments indicated that silence of NEAT1 signally suppressed tumor growth. Taken together, knockdown of NEAT1 suppressed laryngocarcinoma cell growth and metastasis by miR-524-5p/HDAC1/PTEN/AKT signal pathway, which provided a potential therapeutic target for laryngocarcinoma.</description><subject>Acetylation</subject><subject>Adult</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Histone Deacetylase 1 - genetics</subject><subject>Histone Deacetylase 1 - metabolism</subject><subject>Humans</subject><subject>Laryngeal Neoplasms - genetics</subject><subject>Laryngeal Neoplasms - metabolism</subject><subject>Laryngeal Neoplasms - pathology</subject><subject>Male</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>PTEN Phosphohydrolase - chemistry</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>Research Paper</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><issn>1945-4589</issn><issn>1945-4589</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUtP4zAUhS00iEdhyXbk5WwCfsVxNkhVpzykqiBU1pbjOKlHiV3sFA3_hp-KaQsqK1_5Hn_3XB8ALjC6xIJTcqVa69pLgmiBywNwgkuWZywX5a-9-hicxvgPIZ7njB-BY8oELYQoTsD7zLsWOu-0rxMHPs3HcD4dLzC0bmkrO0Q4LA1U2gxvnRqsd9A38HExnaf74NftctPv7VOWE5blK3h193c8wVD9t-mph6vgez-YjSrVnW1M2HKUq9OQVxV30E6FN9ca1UGtnDYBatN18QwcNqqL5nx3jsDzzXQxuctmD7f3k_Es01QUQ1YSXTNaKI4I55Uoq1o3lNU8L3NSVGVDOWLE6KYUuKoxqYypeUMJIogTzBCiI3C95a7WVW9qbdwQVCdXwfbJl_TKyp8dZ5ey9a9ScI44ZgnwZwcI_mVt4iB7Gz9XUM74dZQkOUA4_TtO0mwr1cHHGEzzPQYjuUlVblKV21ST_ve-t2_1V4z0A1mkn1g</recordid><startdate>20211127</startdate><enddate>20211127</enddate><creator>Zhang, Jiajia</creator><creator>Wang, Ping</creator><creator>Cui, Yanli</creator><general>Impact Journals</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><scope>5PM</scope></search><sort><creationdate>20211127</creationdate><title>Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells</title><author>Zhang, Jiajia ; Wang, Ping ; Cui, Yanli</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-92cd437a60266b89bdcf34d659527b9f36042ecf981bd12beed6f320206214003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acetylation</topic><topic>Adult</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>Histone Deacetylase 1 - genetics</topic><topic>Histone Deacetylase 1 - metabolism</topic><topic>Humans</topic><topic>Laryngeal Neoplasms - genetics</topic><topic>Laryngeal Neoplasms - metabolism</topic><topic>Laryngeal Neoplasms - pathology</topic><topic>Male</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>PTEN Phosphohydrolase - chemistry</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>Research Paper</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Jiajia</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><creatorcontrib>Cui, Yanli</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Aging (Albany, NY.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jiajia</au><au>Wang, Ping</au><au>Cui, Yanli</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells</atitle><jtitle>Aging (Albany, NY.)</jtitle><addtitle>Aging (Albany NY)</addtitle><date>2021-11-27</date><risdate>2021</risdate><volume>13</volume><issue>22</issue><spage>24850</spage><epage>24865</epage><pages>24850-24865</pages><issn>1945-4589</issn><eissn>1945-4589</eissn><abstract>Long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is abnormally expressed in numerous tumors and functions as an oncogene, but the role of NEAT1 in laryngocarcinoma is largely unknown. Our study validated that NEAT1 expression was markedly upregulated in laryngocarcinoma tissues and cells. Downregulation of NEAT1 dramatically suppressed cell proliferation and invasion through inhibiting miR-524-5p expression. Additionally, NEAT1 overexpression promoted cell growth and metastasis, while overexpression of miR-524-5p could reverse the effect. NEAT1 increased the expression of histone deacetylase 1 gene (HDAC1) via sponging miR-524-5p. Mechanistically, overexpression of HDAC1 recovered the cancer-inhibiting effects of miR-524-5p mimic or NEAT1 silence by deacetylation of tensin homolog deleted on chromosome ten (PTEN) and inhibiting AKT signal pathway. Moreover, experiments indicated that silence of NEAT1 signally suppressed tumor growth. Taken together, knockdown of NEAT1 suppressed laryngocarcinoma cell growth and metastasis by miR-524-5p/HDAC1/PTEN/AKT signal pathway, which provided a potential therapeutic target for laryngocarcinoma.</abstract><cop>United States</cop><pub>Impact Journals</pub><pmid>34837887</pmid><doi>10.18632/aging.203719</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1945-4589
ispartof Aging (Albany, NY.), 2021-11, Vol.13 (22), p.24850-24865
issn 1945-4589
1945-4589
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8660614
source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; PubMed Central
subjects Acetylation
Adult
Cell Proliferation - genetics
Female
Histone Deacetylase 1 - genetics
Histone Deacetylase 1 - metabolism
Humans
Laryngeal Neoplasms - genetics
Laryngeal Neoplasms - metabolism
Laryngeal Neoplasms - pathology
Male
MicroRNAs - genetics
MicroRNAs - metabolism
Middle Aged
Neoplasm Invasiveness - genetics
PTEN Phosphohydrolase - chemistry
PTEN Phosphohydrolase - genetics
PTEN Phosphohydrolase - metabolism
Research Paper
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
title Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T06%3A57%3A21IST&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=Long%20noncoding%20RNA%20NEAT1%20inhibits%20the%20acetylation%20of%20PTEN%20through%20the%20miR-524-5p%20/HDAC1%20axis%20to%20promote%20the%20proliferation%20and%20invasion%20of%20laryngeal%20cancer%20cells&rft.jtitle=Aging%20(Albany,%20NY.)&rft.au=Zhang,%20Jiajia&rft.date=2021-11-27&rft.volume=13&rft.issue=22&rft.spage=24850&rft.epage=24865&rft.pages=24850-24865&rft.issn=1945-4589&rft.eissn=1945-4589&rft_id=info:doi/10.18632/aging.203719&rft_dat=%3Cproquest_pubme%3E2604018371%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=2604018371&rft_id=info:pmid/34837887&rfr_iscdi=true