Knockdown of lncRNA HIF1A-AS2 increases drug sensitivity of SCLC cells in association with autophagy
The aim of this study was to determine the effect of lncRNA HIF1A-AS2 on autophagy-associated drug resistance in small cell lung cancer (SCLC) cells. The expression of HIF1A-AS2 was silenced by siRNA in doxorubicin-sensitive H69 and doxorubicin-resistant H69AR cells. Then, cytotoxicity, apoptosis an...
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| Veröffentlicht in: | Medical oncology (Northwood, London, England) London, England), 2021-09, Vol.38 (9), p.113-113, Article 113 |
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| creator | Güçlü, Ebru Eroğlu Güneş, Canan Kurar, Ercan Vural, Hasibe |
| description | The aim of this study was to determine the effect of lncRNA HIF1A-AS2 on autophagy-associated drug resistance in small cell lung cancer (SCLC) cells. The expression of HIF1A-AS2 was silenced by siRNA in doxorubicin-sensitive H69 and doxorubicin-resistant H69AR cells. Then, cytotoxicity, apoptosis and autophagy analyses were carried out in the normoxic and CoCl
2
-induced hypoxic environment. The effect of HIF1A-AS2 on the expression levels of genes, which are associated with drug resistance and autophagy, was determinated by qRT-PCR analysis. The levels of MRP1, HIF-1α and Beclin-1 were analyzed by western blot method. Knockdown of HIF1A-AS2 increased doxorubicin sensitivity of SCLC cells and decreased autophagy. Knockdown of HIF1A-AS2 has also affected the expression of several genes that will increase drug sensitivity and inhibit autophagy in both cell lines. The levels of HIF-1α and Beclin-1 were decreased in both cell lines by knockdown of HIF1A-AS2. MRP1 expression was decrease in H69AR cells. In addition, CoCl
2
-induced hypoxic environment decreased in doxorubicin sensitivity of H69 cells, and knockdown of HIF1A-AS2 reversed this effect of hypoxia. Knockdown of HIF1A-AS2 increased drug sensitivity of SCLC cells in relation to autophagy. Therefore, hypoxia-HIF1A-AS2-autophagy interaction is thought to be determinative in drug sensitivity of these cells. |
| doi_str_mv | 10.1007/s12032-021-01562-2 |
| format | Article |
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2
-induced hypoxic environment. The effect of HIF1A-AS2 on the expression levels of genes, which are associated with drug resistance and autophagy, was determinated by qRT-PCR analysis. The levels of MRP1, HIF-1α and Beclin-1 were analyzed by western blot method. Knockdown of HIF1A-AS2 increased doxorubicin sensitivity of SCLC cells and decreased autophagy. Knockdown of HIF1A-AS2 has also affected the expression of several genes that will increase drug sensitivity and inhibit autophagy in both cell lines. The levels of HIF-1α and Beclin-1 were decreased in both cell lines by knockdown of HIF1A-AS2. MRP1 expression was decrease in H69AR cells. In addition, CoCl
2
-induced hypoxic environment decreased in doxorubicin sensitivity of H69 cells, and knockdown of HIF1A-AS2 reversed this effect of hypoxia. Knockdown of HIF1A-AS2 increased drug sensitivity of SCLC cells in relation to autophagy. Therefore, hypoxia-HIF1A-AS2-autophagy interaction is thought to be determinative in drug sensitivity of these cells.</description><identifier>ISSN: 1357-0560</identifier><identifier>EISSN: 1559-131X</identifier><identifier>DOI: 10.1007/s12032-021-01562-2</identifier><identifier>PMID: 34378101</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antibiotics, Antineoplastic - pharmacology ; Apoptosis ; Autophagy ; Biomarkers, Tumor - genetics ; Cell Proliferation ; Doxorubicin - pharmacology ; Drug resistance ; Drug Resistance, Neoplasm - genetics ; Gene Expression Regulation, Neoplastic ; Hematology ; Humans ; Hypoxia ; Internal Medicine ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Medicine ; Medicine & Public Health ; Oncology ; Original Paper ; Pathology ; RNA, Long Noncoding - antagonists & inhibitors ; Small Cell Lung Carcinoma - drug therapy ; Small Cell Lung Carcinoma - genetics ; Small Cell Lung Carcinoma - pathology ; Tumor Cells, Cultured</subject><ispartof>Medical oncology (Northwood, London, England), 2021-09, Vol.38 (9), p.113-113, Article 113</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-e26d8d702c75e8ee2fcc58369a60016c58782392d1088a43581f590e221db5cb3</citedby><cites>FETCH-LOGICAL-c375t-e26d8d702c75e8ee2fcc58369a60016c58782392d1088a43581f590e221db5cb3</cites><orcidid>0000-0001-5330-6159</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12032-021-01562-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12032-021-01562-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34378101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Güçlü, Ebru</creatorcontrib><creatorcontrib>Eroğlu Güneş, Canan</creatorcontrib><creatorcontrib>Kurar, Ercan</creatorcontrib><creatorcontrib>Vural, Hasibe</creatorcontrib><title>Knockdown of lncRNA HIF1A-AS2 increases drug sensitivity of SCLC cells in association with autophagy</title><title>Medical oncology (Northwood, London, England)</title><addtitle>Med Oncol</addtitle><addtitle>Med Oncol</addtitle><description>The aim of this study was to determine the effect of lncRNA HIF1A-AS2 on autophagy-associated drug resistance in small cell lung cancer (SCLC) cells. The expression of HIF1A-AS2 was silenced by siRNA in doxorubicin-sensitive H69 and doxorubicin-resistant H69AR cells. Then, cytotoxicity, apoptosis and autophagy analyses were carried out in the normoxic and CoCl
2
-induced hypoxic environment. The effect of HIF1A-AS2 on the expression levels of genes, which are associated with drug resistance and autophagy, was determinated by qRT-PCR analysis. The levels of MRP1, HIF-1α and Beclin-1 were analyzed by western blot method. Knockdown of HIF1A-AS2 increased doxorubicin sensitivity of SCLC cells and decreased autophagy. Knockdown of HIF1A-AS2 has also affected the expression of several genes that will increase drug sensitivity and inhibit autophagy in both cell lines. The levels of HIF-1α and Beclin-1 were decreased in both cell lines by knockdown of HIF1A-AS2. MRP1 expression was decrease in H69AR cells. In addition, CoCl
2
-induced hypoxic environment decreased in doxorubicin sensitivity of H69 cells, and knockdown of HIF1A-AS2 reversed this effect of hypoxia. Knockdown of HIF1A-AS2 increased drug sensitivity of SCLC cells in relation to autophagy. Therefore, hypoxia-HIF1A-AS2-autophagy interaction is thought to be determinative in drug sensitivity of these cells.</description><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Cell Proliferation</subject><subject>Doxorubicin - pharmacology</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hematology</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Internal Medicine</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>RNA, Long Noncoding - antagonists & inhibitors</subject><subject>Small Cell Lung Carcinoma - drug therapy</subject><subject>Small Cell Lung Carcinoma - genetics</subject><subject>Small Cell Lung Carcinoma - pathology</subject><subject>Tumor Cells, Cultured</subject><issn>1357-0560</issn><issn>1559-131X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU1rGzEQhkVpSNIkf6CHIuilF7WaUbQrHY1pPqhpIB-Qm5C1WkepLbnSboL_feU4baGHnmZgnnlneF9C3gP_DJy3XwogF8g4AuMgG2T4hhyClJqBgPu3tReyZVw2_IC8K-WRV1Ki3icH4lS0Cjgcku5bTO5Hl54jTT1dRnf9fUIvLs9gwiY3SEN02dviC-3yuKDFxxKG8BSGzRa_mc6m1PnlslSQ2lKSC3YIKdLnMDxQOw5p_WAXm2Oy19tl8Sev9YjcnX29nV6w2dX55XQyY060cmAem051LUfXSq-8x945qUSjbcM5NLVvFQqNHXCl7KmQCnqpuUeEbi7dXByRTzvddU4_R18Gswpl-5-NPo3FYLUCtWo0VPTjP-hjGnOs31VKai1504pK4Y5yOZWSfW_WOaxs3hjgZpuB2WVgqrPmJQODdenDq_Q4X_nuz8pv0ysgdkCpo7jw-e_t_8j-Agwcjz4</recordid><startdate>20210901</startdate><enddate>20210901</enddate><creator>Güçlü, Ebru</creator><creator>Eroğlu Güneş, Canan</creator><creator>Kurar, Ercan</creator><creator>Vural, Hasibe</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5330-6159</orcidid></search><sort><creationdate>20210901</creationdate><title>Knockdown of lncRNA HIF1A-AS2 increases drug sensitivity of SCLC cells in association with autophagy</title><author>Güçlü, Ebru ; Eroğlu Güneş, Canan ; Kurar, Ercan ; Vural, Hasibe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-e26d8d702c75e8ee2fcc58369a60016c58782392d1088a43581f590e221db5cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Cell Proliferation</topic><topic>Doxorubicin - pharmacology</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hematology</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Internal Medicine</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>RNA, Long Noncoding - antagonists & inhibitors</topic><topic>Small Cell Lung Carcinoma - drug therapy</topic><topic>Small Cell Lung Carcinoma - genetics</topic><topic>Small Cell Lung Carcinoma - pathology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Güçlü, Ebru</creatorcontrib><creatorcontrib>Eroğlu Güneş, Canan</creatorcontrib><creatorcontrib>Kurar, Ercan</creatorcontrib><creatorcontrib>Vural, Hasibe</creatorcontrib><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>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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</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>Medical 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>MEDLINE - Academic</collection><jtitle>Medical oncology (Northwood, London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Güçlü, Ebru</au><au>Eroğlu Güneş, Canan</au><au>Kurar, Ercan</au><au>Vural, Hasibe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockdown of lncRNA HIF1A-AS2 increases drug sensitivity of SCLC cells in association with autophagy</atitle><jtitle>Medical oncology (Northwood, London, England)</jtitle><stitle>Med Oncol</stitle><addtitle>Med Oncol</addtitle><date>2021-09-01</date><risdate>2021</risdate><volume>38</volume><issue>9</issue><spage>113</spage><epage>113</epage><pages>113-113</pages><artnum>113</artnum><issn>1357-0560</issn><eissn>1559-131X</eissn><abstract>The aim of this study was to determine the effect of lncRNA HIF1A-AS2 on autophagy-associated drug resistance in small cell lung cancer (SCLC) cells. The expression of HIF1A-AS2 was silenced by siRNA in doxorubicin-sensitive H69 and doxorubicin-resistant H69AR cells. Then, cytotoxicity, apoptosis and autophagy analyses were carried out in the normoxic and CoCl
2
-induced hypoxic environment. The effect of HIF1A-AS2 on the expression levels of genes, which are associated with drug resistance and autophagy, was determinated by qRT-PCR analysis. The levels of MRP1, HIF-1α and Beclin-1 were analyzed by western blot method. Knockdown of HIF1A-AS2 increased doxorubicin sensitivity of SCLC cells and decreased autophagy. Knockdown of HIF1A-AS2 has also affected the expression of several genes that will increase drug sensitivity and inhibit autophagy in both cell lines. The levels of HIF-1α and Beclin-1 were decreased in both cell lines by knockdown of HIF1A-AS2. MRP1 expression was decrease in H69AR cells. In addition, CoCl
2
-induced hypoxic environment decreased in doxorubicin sensitivity of H69 cells, and knockdown of HIF1A-AS2 reversed this effect of hypoxia. Knockdown of HIF1A-AS2 increased drug sensitivity of SCLC cells in relation to autophagy. Therefore, hypoxia-HIF1A-AS2-autophagy interaction is thought to be determinative in drug sensitivity of these cells.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34378101</pmid><doi>10.1007/s12032-021-01562-2</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-5330-6159</orcidid></addata></record> |
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| ispartof | Medical oncology (Northwood, London, England), 2021-09, Vol.38 (9), p.113-113, Article 113 |
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| subjects | Antibiotics, Antineoplastic - pharmacology Apoptosis Autophagy Biomarkers, Tumor - genetics Cell Proliferation Doxorubicin - pharmacology Drug resistance Drug Resistance, Neoplasm - genetics Gene Expression Regulation, Neoplastic Hematology Humans Hypoxia Internal Medicine Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - pathology Medicine Medicine & Public Health Oncology Original Paper Pathology RNA, Long Noncoding - antagonists & inhibitors Small Cell Lung Carcinoma - drug therapy Small Cell Lung Carcinoma - genetics Small Cell Lung Carcinoma - pathology Tumor Cells, Cultured |
| title | Knockdown of lncRNA HIF1A-AS2 increases drug sensitivity of SCLC cells in association with autophagy |
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