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Long noncoding RNA MALAT1 inhibits the apoptosis and autophagy of hepatocellular carcinoma cell by targeting the microRNA-146a/PI3K/Akt/mTOR axis
Increased long noncoding RNA (lncRNA) expression is characteristic to hepatocellular carcinoma (HCC) and several other neoplasms. The present study aimed to identify the mechanism underlying modulation of HCC development by the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)....
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Published in: | Cancer cell international 2020-05, Vol.20 (1), p.165-165, Article 165 |
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description | Increased long noncoding RNA (lncRNA) expression is characteristic to hepatocellular carcinoma (HCC) and several other neoplasms. The present study aimed to identify the mechanism underlying modulation of HCC development by the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1).
Quantitative real-time polymerase chain reaction was used to determine MALAT1 and microRNA (miR)-146a expression in HCC tissues and cell lines. Western blotting was performed to measure PI3K, Akt, and mTOR levels. Dual-luciferase reporter assay was used to validate the direct targeting and negative regulatory interaction between miR-146a and MALAT1. Cell viability, proliferation, and apoptosis were analyzed using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, colony formation assay, and flow cytometry, respectively; autophagy was detected based on LC3B expression.
MALAT1 expression was higher in HCC tissues than in normal tissues. MALAT1 upregulation promoted HCC cell proliferation, whereas MALAT1 downregulation promoted HCC apoptosis and autophagy. Moreover, effects of MALAT1 downregulation on HCC cells were abolished by miR-146a inhibition. miR-146a directly targeted the 3'-untranslated region of
, and PI3K protein level was clearly decreased upon miR-146a mimic transfection.
MALAT1 may modulate HCC cell proliferation, apoptosis, and autophagy via sponging miR-146a, which regulates HCC progression. |
doi_str_mv | 10.1186/s12935-020-01231-w |
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Quantitative real-time polymerase chain reaction was used to determine MALAT1 and microRNA (miR)-146a expression in HCC tissues and cell lines. Western blotting was performed to measure PI3K, Akt, and mTOR levels. Dual-luciferase reporter assay was used to validate the direct targeting and negative regulatory interaction between miR-146a and MALAT1. Cell viability, proliferation, and apoptosis were analyzed using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, colony formation assay, and flow cytometry, respectively; autophagy was detected based on LC3B expression.
MALAT1 expression was higher in HCC tissues than in normal tissues. MALAT1 upregulation promoted HCC cell proliferation, whereas MALAT1 downregulation promoted HCC apoptosis and autophagy. Moreover, effects of MALAT1 downregulation on HCC cells were abolished by miR-146a inhibition. miR-146a directly targeted the 3'-untranslated region of
, and PI3K protein level was clearly decreased upon miR-146a mimic transfection.
MALAT1 may modulate HCC cell proliferation, apoptosis, and autophagy via sponging miR-146a, which regulates HCC progression.</description><identifier>ISSN: 1475-2867</identifier><identifier>EISSN: 1475-2867</identifier><identifier>DOI: 10.1186/s12935-020-01231-w</identifier><identifier>PMID: 32435156</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>1-Phosphatidylinositol 3-kinase ; Adenocarcinoma ; AKT protein ; Apoptosis ; Autophagy ; Cancer therapies ; Cell cycle ; Cell proliferation ; Cell viability ; Flow cytometry ; HCC ; Hepatocellular carcinoma ; Kinases ; Liver cancer ; lncRNA ; Lung cancer ; Medical prognosis ; Metastases ; Metastasis ; MicroRNAs ; miR ; miRNA ; Neoplasia ; Phagocytosis ; PI3K ; Polymerase chain reaction ; Primary Research ; Proteins ; TOR protein ; Transcription ; Transfection ; Western blotting</subject><ispartof>Cancer cell international, 2020-05, Vol.20 (1), p.165-165, Article 165</ispartof><rights>The Author(s) 2020.</rights><rights>2020. This work is licensed 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><rights>The Author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c597t-4cff3035d82fd45fdaccc827d9b10d33990d2e208611776aa96ad79afa979c6d3</citedby><cites>FETCH-LOGICAL-c597t-4cff3035d82fd45fdaccc827d9b10d33990d2e208611776aa96ad79afa979c6d3</cites><orcidid>0000-0001-8683-4978</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/PMC7222315/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2404430584?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32435156$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Peng, Ningfu</creatorcontrib><creatorcontrib>He, Jingrong</creatorcontrib><creatorcontrib>Li, Jindu</creatorcontrib><creatorcontrib>Huang, Hao</creatorcontrib><creatorcontrib>Huang, Weiqiao</creatorcontrib><creatorcontrib>Liao, Yingyang</creatorcontrib><creatorcontrib>Zhu, Shaoliang</creatorcontrib><title>Long noncoding RNA MALAT1 inhibits the apoptosis and autophagy of hepatocellular carcinoma cell by targeting the microRNA-146a/PI3K/Akt/mTOR axis</title><title>Cancer cell international</title><addtitle>Cancer Cell Int</addtitle><description>Increased long noncoding RNA (lncRNA) expression is characteristic to hepatocellular carcinoma (HCC) and several other neoplasms. The present study aimed to identify the mechanism underlying modulation of HCC development by the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1).
Quantitative real-time polymerase chain reaction was used to determine MALAT1 and microRNA (miR)-146a expression in HCC tissues and cell lines. Western blotting was performed to measure PI3K, Akt, and mTOR levels. Dual-luciferase reporter assay was used to validate the direct targeting and negative regulatory interaction between miR-146a and MALAT1. Cell viability, proliferation, and apoptosis were analyzed using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, colony formation assay, and flow cytometry, respectively; autophagy was detected based on LC3B expression.
MALAT1 expression was higher in HCC tissues than in normal tissues. MALAT1 upregulation promoted HCC cell proliferation, whereas MALAT1 downregulation promoted HCC apoptosis and autophagy. Moreover, effects of MALAT1 downregulation on HCC cells were abolished by miR-146a inhibition. miR-146a directly targeted the 3'-untranslated region of
, and PI3K protein level was clearly decreased upon miR-146a mimic transfection.
MALAT1 may modulate HCC cell proliferation, apoptosis, and autophagy via sponging miR-146a, which regulates HCC progression.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Adenocarcinoma</subject><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell proliferation</subject><subject>Cell viability</subject><subject>Flow cytometry</subject><subject>HCC</subject><subject>Hepatocellular carcinoma</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>lncRNA</subject><subject>Lung cancer</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>miR</subject><subject>miRNA</subject><subject>Neoplasia</subject><subject>Phagocytosis</subject><subject>PI3K</subject><subject>Polymerase chain reaction</subject><subject>Primary Research</subject><subject>Proteins</subject><subject>TOR protein</subject><subject>Transcription</subject><subject>Transfection</subject><subject>Western blotting</subject><issn>1475-2867</issn><issn>1475-2867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdks1u1DAUhSMEoqXwAiyQJTZswvgvdrJBGlUURgwUVcPaurGdGQ9JHGyHdh6DNybplKpl5avrcz_bxyfLXhP8npBSLCKhFStyTHGOCWUkv36SnRIui5yWQj59UJ9kL2LcY0xkKfDz7IRRzgpSiNPsz9r3W9T7Xnvjpurq2xJ9Xa6XG4Jcv3O1SxGlnUUw-CH56CKC3iAYkx92sD0g36CdHSB5bdt2bCEgDUG73neA5haqDyhB2No002dS53Tw0zE54QIW31fsy2L5My26zeUVghsXX2bPGmijfXW3nmU_Lj5uzj_n68tPq_PlOtdFJVPOddMwzApT0sbwojGgtS6pNFVNsGGsqrChluJSECKlAKgEGFlBA5WstDDsLFsducbDXg3BdRAOyoNTtw0ftgpCcrq1qobaMqttUTLgDUBdW6y1rCtBNbeimFgfjqxhrDtrtO1TgPYR9PFO73Zq638rSen0cTPg3R0g-F-jjUl1Ls7-QW_9GBXluGBMkpJO0rf_Sfd-DP1k1azinOGi5JOKHlWT2TEG29xfhmA1p0cd06Om9Kjb9KjraejNw2fcj_yLC_sLdMrCFA</recordid><startdate>20200513</startdate><enddate>20200513</enddate><creator>Peng, Ningfu</creator><creator>He, Jingrong</creator><creator>Li, Jindu</creator><creator>Huang, Hao</creator><creator>Huang, Weiqiao</creator><creator>Liao, Yingyang</creator><creator>Zhu, Shaoliang</creator><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-8683-4978</orcidid></search><sort><creationdate>20200513</creationdate><title>Long noncoding RNA MALAT1 inhibits the apoptosis and autophagy of hepatocellular carcinoma cell by targeting the microRNA-146a/PI3K/Akt/mTOR axis</title><author>Peng, Ningfu ; 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The present study aimed to identify the mechanism underlying modulation of HCC development by the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1).
Quantitative real-time polymerase chain reaction was used to determine MALAT1 and microRNA (miR)-146a expression in HCC tissues and cell lines. Western blotting was performed to measure PI3K, Akt, and mTOR levels. Dual-luciferase reporter assay was used to validate the direct targeting and negative regulatory interaction between miR-146a and MALAT1. Cell viability, proliferation, and apoptosis were analyzed using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, colony formation assay, and flow cytometry, respectively; autophagy was detected based on LC3B expression.
MALAT1 expression was higher in HCC tissues than in normal tissues. MALAT1 upregulation promoted HCC cell proliferation, whereas MALAT1 downregulation promoted HCC apoptosis and autophagy. Moreover, effects of MALAT1 downregulation on HCC cells were abolished by miR-146a inhibition. miR-146a directly targeted the 3'-untranslated region of
, and PI3K protein level was clearly decreased upon miR-146a mimic transfection.
MALAT1 may modulate HCC cell proliferation, apoptosis, and autophagy via sponging miR-146a, which regulates HCC progression.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>32435156</pmid><doi>10.1186/s12935-020-01231-w</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-8683-4978</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase Adenocarcinoma AKT protein Apoptosis Autophagy Cancer therapies Cell cycle Cell proliferation Cell viability Flow cytometry HCC Hepatocellular carcinoma Kinases Liver cancer lncRNA Lung cancer Medical prognosis Metastases Metastasis MicroRNAs miR miRNA Neoplasia Phagocytosis PI3K Polymerase chain reaction Primary Research Proteins TOR protein Transcription Transfection Western blotting |
title | Long noncoding RNA MALAT1 inhibits the apoptosis and autophagy of hepatocellular carcinoma cell by targeting the microRNA-146a/PI3K/Akt/mTOR axis |
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