Propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR/p70S6K signaling pathway in melanoma cells
Propofol is an intravenous anesthetic, which is widely used in clinical anesthesia induction and maintenance and is critical in the sedation of patients. However, the functions and mechanisms of propofol on apoptosis of melanoma cells remain unclear. The present study investigated whether propofol p...
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| Veröffentlicht in: | Oncology letters 2018-01, Vol.15 (1), p.630-634 |
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| creator | Shang, Zhiwei Feng, Haixia Cui, Lisha Wang, Weiping Fu, Hongwei |
| description | Propofol is an intravenous anesthetic, which is widely used in clinical anesthesia induction and maintenance and is critical in the sedation of patients. However, the functions and mechanisms of propofol on apoptosis of melanoma cells remain unclear. The present study investigated whether propofol promotes cell apoptosis and suppresses the HOX transcript antisense RNA (HOTAIR)-mediated mechanistic target of rapamycin (mTOR) pathway in melanoma cells. B16F10 cells were cultured with different concentrations (0-10 µM) of propofol for 24 or 48 h. Proliferation and apoptosis of B16F10 cells were detected using MTT assay and flow cytometry. The pcDNA 3.1(-)-HOTAIR and pcDNA 3.1(-)-control plasmids were transfected into B16F10 cells using Lipofectamine 2000. In the present study, treatment with propofol significantly reduced viability, and induced apoptosis and caspase-3 activity in melanoma cells. Propofol treatment significantly inhibited HOTAIR expression and the expression of phosphorylated (p)-mTOR and p- p70S6K protein in melanoma cells. Overexpression of HOTAIR significantly increased viability of melanoma cells, and increased HOTAIR, p-mTOR and p-p70S6K protein expression in melanoma cells. These results indicated that propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR signaling pathway in melanoma cells. |
| doi_str_mv | 10.3892/ol.2017.7297 |
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However, the functions and mechanisms of propofol on apoptosis of melanoma cells remain unclear. The present study investigated whether propofol promotes cell apoptosis and suppresses the HOX transcript antisense RNA (HOTAIR)-mediated mechanistic target of rapamycin (mTOR) pathway in melanoma cells. B16F10 cells were cultured with different concentrations (0-10 µM) of propofol for 24 or 48 h. Proliferation and apoptosis of B16F10 cells were detected using MTT assay and flow cytometry. The pcDNA 3.1(-)-HOTAIR and pcDNA 3.1(-)-control plasmids were transfected into B16F10 cells using Lipofectamine 2000. In the present study, treatment with propofol significantly reduced viability, and induced apoptosis and caspase-3 activity in melanoma cells. Propofol treatment significantly inhibited HOTAIR expression and the expression of phosphorylated (p)-mTOR and p- p70S6K protein in melanoma cells. Overexpression of HOTAIR significantly increased viability of melanoma cells, and increased HOTAIR, p-mTOR and p-p70S6K protein expression in melanoma cells. These results indicated that propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR signaling pathway in melanoma cells.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2017.7297</identifier><identifier>PMID: 29375720</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Autophagy ; Biotechnology ; Breast cancer ; Care and treatment ; Cell cycle ; Cell growth ; Cellular signal transduction ; Development and progression ; Genetic aspects ; Health aspects ; Kinases ; Liver cancer ; Melanoma ; Metastasis ; Oncology ; Patient outcomes ; Phosphorylation ; Plasmids ; Propofol ; Protein expression ; Proteins ; Signal transduction ; Skin cancer ; Statistical analysis ; Transcription factors ; Tumors</subject><ispartof>Oncology letters, 2018-01, Vol.15 (1), p.630-634</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright © 2018, Spandidos Publications 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-be60b419e8f02e92725fa20d81e831bd7a3377a6db9884a13e0a48a84e31374d3</citedby><cites>FETCH-LOGICAL-c510t-be60b419e8f02e92725fa20d81e831bd7a3377a6db9884a13e0a48a84e31374d3</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/PMC5766068/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5766068/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29375720$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shang, Zhiwei</creatorcontrib><creatorcontrib>Feng, Haixia</creatorcontrib><creatorcontrib>Cui, Lisha</creatorcontrib><creatorcontrib>Wang, Weiping</creatorcontrib><creatorcontrib>Fu, Hongwei</creatorcontrib><title>Propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR/p70S6K signaling pathway in melanoma cells</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>Propofol is an intravenous anesthetic, which is widely used in clinical anesthesia induction and maintenance and is critical in the sedation of patients. However, the functions and mechanisms of propofol on apoptosis of melanoma cells remain unclear. The present study investigated whether propofol promotes cell apoptosis and suppresses the HOX transcript antisense RNA (HOTAIR)-mediated mechanistic target of rapamycin (mTOR) pathway in melanoma cells. B16F10 cells were cultured with different concentrations (0-10 µM) of propofol for 24 or 48 h. Proliferation and apoptosis of B16F10 cells were detected using MTT assay and flow cytometry. The pcDNA 3.1(-)-HOTAIR and pcDNA 3.1(-)-control plasmids were transfected into B16F10 cells using Lipofectamine 2000. In the present study, treatment with propofol significantly reduced viability, and induced apoptosis and caspase-3 activity in melanoma cells. Propofol treatment significantly inhibited HOTAIR expression and the expression of phosphorylated (p)-mTOR and p- p70S6K protein in melanoma cells. Overexpression of HOTAIR significantly increased viability of melanoma cells, and increased HOTAIR, p-mTOR and p-p70S6K protein expression in melanoma cells. These results indicated that propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR signaling pathway in melanoma cells.</description><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Biotechnology</subject><subject>Breast cancer</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cellular signal transduction</subject><subject>Development and progression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Melanoma</subject><subject>Metastasis</subject><subject>Oncology</subject><subject>Patient outcomes</subject><subject>Phosphorylation</subject><subject>Plasmids</subject><subject>Propofol</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Skin cancer</subject><subject>Statistical analysis</subject><subject>Transcription factors</subject><subject>Tumors</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk1v1DAQhiMEolXpjTOKhIQ4kK0_En9ckFYVpRWVFpXlbDnJZOPKsYOdgPrv69CydBH2wSPPM-_YozfLXmO0okKSM29XBGG-4kTyZ9kx5pIUGAnyfB_z8ig7jfEWpVUxLAR7mR0RSXnFCTrO3NfgR995m4_BD36CmOvRj5OPJkWuzeM8jgFiTImph_xys11f3RQDtEZP0ObDdnNzNnL0jX3Jo9k5bY3b5aOe-l_6LjcuH8Bq5wedN2BtfJW96LSNcPp4nmTfLz5tzy-L683nq_P1ddFUGE1FDQzVJZYgOkRAEk6qThPUCgyC4rrlmlLONWtrKUSpMQWkS6FFCRRTXrb0JPv4oDvOdXprA24K2qoxmEGHO-W1UYcZZ3q18z9VxRlDTCSB948Cwf-YIU5qMHH5gnbg56iwlBRhjJhM6Nt_0Fs_hzSJ35RkmEnC_lI7bUEZ1_nUt1lE1boiQjIkOE3U6j9U2i0MpvEOOpPuDwrePSnoQdupj97Ok_EuHoIfHsAm-BgDdPthYKQWLylv1eIltXgp4W-eDnAP_3EOvQedVcKH</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Shang, Zhiwei</creator><creator>Feng, Haixia</creator><creator>Cui, Lisha</creator><creator>Wang, Weiping</creator><creator>Fu, Hongwei</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180101</creationdate><title>Propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR/p70S6K signaling pathway in melanoma cells</title><author>Shang, Zhiwei ; Feng, Haixia ; Cui, Lisha ; Wang, Weiping ; Fu, Hongwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-be60b419e8f02e92725fa20d81e831bd7a3377a6db9884a13e0a48a84e31374d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Biotechnology</topic><topic>Breast cancer</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cellular signal transduction</topic><topic>Development and progression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Melanoma</topic><topic>Metastasis</topic><topic>Oncology</topic><topic>Patient outcomes</topic><topic>Phosphorylation</topic><topic>Plasmids</topic><topic>Propofol</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Skin cancer</topic><topic>Statistical analysis</topic><topic>Transcription factors</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Shang, Zhiwei</creatorcontrib><creatorcontrib>Feng, Haixia</creatorcontrib><creatorcontrib>Cui, Lisha</creatorcontrib><creatorcontrib>Wang, Weiping</creatorcontrib><creatorcontrib>Fu, Hongwei</creatorcontrib><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>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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shang, Zhiwei</au><au>Feng, Haixia</au><au>Cui, Lisha</au><au>Wang, Weiping</au><au>Fu, Hongwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR/p70S6K signaling pathway in melanoma cells</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>15</volume><issue>1</issue><spage>630</spage><epage>634</epage><pages>630-634</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>Propofol is an intravenous anesthetic, which is widely used in clinical anesthesia induction and maintenance and is critical in the sedation of patients. However, the functions and mechanisms of propofol on apoptosis of melanoma cells remain unclear. The present study investigated whether propofol promotes cell apoptosis and suppresses the HOX transcript antisense RNA (HOTAIR)-mediated mechanistic target of rapamycin (mTOR) pathway in melanoma cells. B16F10 cells were cultured with different concentrations (0-10 µM) of propofol for 24 or 48 h. Proliferation and apoptosis of B16F10 cells were detected using MTT assay and flow cytometry. The pcDNA 3.1(-)-HOTAIR and pcDNA 3.1(-)-control plasmids were transfected into B16F10 cells using Lipofectamine 2000. In the present study, treatment with propofol significantly reduced viability, and induced apoptosis and caspase-3 activity in melanoma cells. Propofol treatment significantly inhibited HOTAIR expression and the expression of phosphorylated (p)-mTOR and p- p70S6K protein in melanoma cells. Overexpression of HOTAIR significantly increased viability of melanoma cells, and increased HOTAIR, p-mTOR and p-p70S6K protein expression in melanoma cells. These results indicated that propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR signaling pathway in melanoma cells.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29375720</pmid><doi>10.3892/ol.2017.7297</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Apoptosis Autophagy Biotechnology Breast cancer Care and treatment Cell cycle Cell growth Cellular signal transduction Development and progression Genetic aspects Health aspects Kinases Liver cancer Melanoma Metastasis Oncology Patient outcomes Phosphorylation Plasmids Propofol Protein expression Proteins Signal transduction Skin cancer Statistical analysis Transcription factors Tumors |
| title | Propofol promotes apoptosis and suppresses the HOTAIR-mediated mTOR/p70S6K signaling pathway in melanoma cells |
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