The Tumor Suppressor, p53, Contributes to Radiosensitivity of Lung Cancer Cells by Regulating Autophagy and Apoptosis
Cell death is one of the most important endpoints of radiosensitivity. The tumor suppressor p53 participates not only in regulation of apoptosis, but also in autophagy mechanism. In this study, H1299-P53 (with wild-type p53) and H1299-175H (with mutant 175H) were used, and the effects of p53 on radi...
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| Veröffentlicht in: | Cancer biotherapy & radiopharmaceuticals 2013-03, Vol.28 (2), p.153-159 |
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| creator | Cheng, Guanghui Kong, Dejuan Hou, Xue Liang, Bing He, Mengzi Liang, Nan Ma, Shumei Liu, Xiaodong |
| description | Cell death is one of the most important endpoints of radiosensitivity. The tumor suppressor p53 participates not only in regulation of apoptosis, but also in autophagy mechanism. In this study, H1299-P53 (with wild-type p53) and H1299-175H (with mutant 175H) were used, and the effects of p53 on radiosensitivity were analyzed.
Cell models with different p53 status were established by gene engineering, and cell viability was examined by colony formation assay, and cell counting kit-8 (CCK-8), 3-Methyladenine, and Z-VAD were used to block autophagy and apoptosis, respectively. Western blot was used to detect protein expression; monodansylcadaverine (MDC) staining was used to analyze autophagy rate; DAPI/Propidium Iodide (PI) staining and flow cytometry were used to assess apoptosis and necrosis.
In parental H1299, H1299-P53, and H1299-175H cells, radiosensitivity exhibited different by colony formation and CCK-8 assay (D0: 1.764 Gy, 1.407 Gy and 1.695 Gy; Dq: 2.977 Gy, 1.199 Gy and 2.312 Gy in turn). The radiosensitization of p53 was associated with the increase of MDM2 and P21 expression. The ionizing radiation (IR)-induced apoptosis was significant in H1299-P53 compared with in H1299 and H199-175H (p < 0.05) by flow cytometry, and the expression of cleaved-caspase3 was increased in H1299-P53 cells. While the IR-induced autophagy was significant in H1299 cells (p < 0.01) and decreased in H1299-P53 and H1299-175H cells (p < 0.01) by MDC staining, the expression of MAPLC3II and Beclin-1 increased in H1299, but not in H1299-p53 and H199-175H cells. The IR-induced cell survival was significantly increased by Z-VAD-FMK and decreased by 3MA in H1299-P53 cells; IR- induced autophagy was significantly increased by Z-VAD-FMK in H1299-P53 cells (p < 0.01), but not changed in H1299 cells.
p53 could regulate radiosensitivity by inhibiting autophagy and activating apoptosis; autophagy provides a prosurvival mechanism, and p53 potently abrogated the IR-induced autophagy, while mutant 175H shown no effect on radiosensitivity, suggesting that individual treatment strategies should be based on p53 status in patients. |
| doi_str_mv | 10.1089/cbr.2012.1297 |
| format | Article |
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Cell models with different p53 status were established by gene engineering, and cell viability was examined by colony formation assay, and cell counting kit-8 (CCK-8), 3-Methyladenine, and Z-VAD were used to block autophagy and apoptosis, respectively. Western blot was used to detect protein expression; monodansylcadaverine (MDC) staining was used to analyze autophagy rate; DAPI/Propidium Iodide (PI) staining and flow cytometry were used to assess apoptosis and necrosis.
In parental H1299, H1299-P53, and H1299-175H cells, radiosensitivity exhibited different by colony formation and CCK-8 assay (D0: 1.764 Gy, 1.407 Gy and 1.695 Gy; Dq: 2.977 Gy, 1.199 Gy and 2.312 Gy in turn). The radiosensitization of p53 was associated with the increase of MDM2 and P21 expression. The ionizing radiation (IR)-induced apoptosis was significant in H1299-P53 compared with in H1299 and H199-175H (p < 0.05) by flow cytometry, and the expression of cleaved-caspase3 was increased in H1299-P53 cells. While the IR-induced autophagy was significant in H1299 cells (p < 0.01) and decreased in H1299-P53 and H1299-175H cells (p < 0.01) by MDC staining, the expression of MAPLC3II and Beclin-1 increased in H1299, but not in H1299-p53 and H199-175H cells. The IR-induced cell survival was significantly increased by Z-VAD-FMK and decreased by 3MA in H1299-P53 cells; IR- induced autophagy was significantly increased by Z-VAD-FMK in H1299-P53 cells (p < 0.01), but not changed in H1299 cells.
p53 could regulate radiosensitivity by inhibiting autophagy and activating apoptosis; autophagy provides a prosurvival mechanism, and p53 potently abrogated the IR-induced autophagy, while mutant 175H shown no effect on radiosensitivity, suggesting that individual treatment strategies should be based on p53 status in patients.</description><identifier>ISSN: 1084-9785</identifier><identifier>EISSN: 1557-8852</identifier><identifier>DOI: 10.1089/cbr.2012.1297</identifier><identifier>PMID: 23268708</identifier><identifier>CODEN: CBRAFJ</identifier><language>eng</language><publisher>New Rochelle, NY: Liebert</publisher><subject>Apoptosis - radiation effects ; Autophagy - radiation effects ; Biological and medical sciences ; Blotting, Western ; Colony-Forming Units Assay ; Humans ; Lung cancer ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Lung Neoplasms - radiotherapy ; Medical sciences ; Original ; Pneumology ; Radiation therapy and radiosensitizing agent ; Radiation Tolerance - physiology ; Transcriptional Activation ; Treatment with physical agents ; Treatment. General aspects ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; Tumors of the respiratory system and mediastinum ; X-Rays</subject><ispartof>Cancer biotherapy & radiopharmaceuticals, 2013-03, Vol.28 (2), p.153-159</ispartof><rights>2014 INIST-CNRS</rights><rights>(©) Copyright 2013, Mary Ann Liebert, Inc.</rights><rights>Copyright 2013, Mary Ann Liebert, Inc. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-fa56be645318ae49a33d83de7bad5de32897df2b8b7931af85f3ae9a2576afb93</citedby><cites>FETCH-LOGICAL-c511t-fa56be645318ae49a33d83de7bad5de32897df2b8b7931af85f3ae9a2576afb93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27146857$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23268708$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Guanghui</creatorcontrib><creatorcontrib>Kong, Dejuan</creatorcontrib><creatorcontrib>Hou, Xue</creatorcontrib><creatorcontrib>Liang, Bing</creatorcontrib><creatorcontrib>He, Mengzi</creatorcontrib><creatorcontrib>Liang, Nan</creatorcontrib><creatorcontrib>Ma, Shumei</creatorcontrib><creatorcontrib>Liu, Xiaodong</creatorcontrib><title>The Tumor Suppressor, p53, Contributes to Radiosensitivity of Lung Cancer Cells by Regulating Autophagy and Apoptosis</title><title>Cancer biotherapy & radiopharmaceuticals</title><addtitle>Cancer Biother Radiopharm</addtitle><description>Cell death is one of the most important endpoints of radiosensitivity. The tumor suppressor p53 participates not only in regulation of apoptosis, but also in autophagy mechanism. In this study, H1299-P53 (with wild-type p53) and H1299-175H (with mutant 175H) were used, and the effects of p53 on radiosensitivity were analyzed.
Cell models with different p53 status were established by gene engineering, and cell viability was examined by colony formation assay, and cell counting kit-8 (CCK-8), 3-Methyladenine, and Z-VAD were used to block autophagy and apoptosis, respectively. Western blot was used to detect protein expression; monodansylcadaverine (MDC) staining was used to analyze autophagy rate; DAPI/Propidium Iodide (PI) staining and flow cytometry were used to assess apoptosis and necrosis.
In parental H1299, H1299-P53, and H1299-175H cells, radiosensitivity exhibited different by colony formation and CCK-8 assay (D0: 1.764 Gy, 1.407 Gy and 1.695 Gy; Dq: 2.977 Gy, 1.199 Gy and 2.312 Gy in turn). The radiosensitization of p53 was associated with the increase of MDM2 and P21 expression. The ionizing radiation (IR)-induced apoptosis was significant in H1299-P53 compared with in H1299 and H199-175H (p < 0.05) by flow cytometry, and the expression of cleaved-caspase3 was increased in H1299-P53 cells. While the IR-induced autophagy was significant in H1299 cells (p < 0.01) and decreased in H1299-P53 and H1299-175H cells (p < 0.01) by MDC staining, the expression of MAPLC3II and Beclin-1 increased in H1299, but not in H1299-p53 and H199-175H cells. The IR-induced cell survival was significantly increased by Z-VAD-FMK and decreased by 3MA in H1299-P53 cells; IR- induced autophagy was significantly increased by Z-VAD-FMK in H1299-P53 cells (p < 0.01), but not changed in H1299 cells.
p53 could regulate radiosensitivity by inhibiting autophagy and activating apoptosis; autophagy provides a prosurvival mechanism, and p53 potently abrogated the IR-induced autophagy, while mutant 175H shown no effect on radiosensitivity, suggesting that individual treatment strategies should be based on p53 status in patients.</description><subject>Apoptosis - radiation effects</subject><subject>Autophagy - radiation effects</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Colony-Forming Units Assay</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Lung Neoplasms - radiotherapy</subject><subject>Medical sciences</subject><subject>Original</subject><subject>Pneumology</subject><subject>Radiation therapy and radiosensitizing agent</subject><subject>Radiation Tolerance - physiology</subject><subject>Transcriptional Activation</subject><subject>Treatment with physical agents</subject><subject>Treatment. General aspects</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>Tumors of the respiratory system and mediastinum</subject><subject>X-Rays</subject><issn>1084-9785</issn><issn>1557-8852</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><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>eNpdkUtrGzEURofS0KRpl90WQSl0kXGkkfXaBMzQFxgCibsWVzMaW2E8muoR8L-vTNz0sboX7uHjfpyqekfwgmCprjsTFg0mzYI0SryoLghjopaSNS_LjuWyVkKy8-p1jA8YY465eFWdN7ThUmB5UeXNzqJN3vuA7vM8BxujD1doZvQKtX5KwZmcbETJozvonY92ii65R5cOyA9onactamHqbECtHceIzAHd2W0eIblyWuXk5x1sDwimHq1mPycfXXxTnQ0wRvv2NC-rH18-b9pv9fr26_d2ta47RkiqB2DcWL5klEiwSwWU9pL2VhjoWW9pI5Xoh8ZIIxQlMEg2ULAKGiY4DEbRy-rmKXfOZm_7zpZCMOo5uD2Eg_bg9L-Xye301j9qyqSSUpaAT6eA4H9mG5Peu9iVojBZn6MmlDByhHFBP_yHPvgcplKvUJxTxhTjhaqfqC74GIMdnp8hWB-F6iJUH4Xqo9DCv_-7wTP922ABPp4AiB2MQygyXPzDCbLkkgn6C8Dtqxg</recordid><startdate>20130301</startdate><enddate>20130301</enddate><creator>Cheng, Guanghui</creator><creator>Kong, Dejuan</creator><creator>Hou, Xue</creator><creator>Liang, Bing</creator><creator>He, Mengzi</creator><creator>Liang, Nan</creator><creator>Ma, Shumei</creator><creator>Liu, Xiaodong</creator><general>Liebert</general><general>Mary Ann Liebert, Inc</general><scope>IQODW</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8C1</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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130301</creationdate><title>The Tumor Suppressor, p53, Contributes to Radiosensitivity of Lung Cancer Cells by Regulating Autophagy and Apoptosis</title><author>Cheng, Guanghui ; Kong, Dejuan ; Hou, Xue ; Liang, Bing ; He, Mengzi ; Liang, Nan ; Ma, Shumei ; Liu, Xiaodong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-fa56be645318ae49a33d83de7bad5de32897df2b8b7931af85f3ae9a2576afb93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Apoptosis - radiation effects</topic><topic>Autophagy - radiation effects</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Colony-Forming Units Assay</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Lung Neoplasms - radiotherapy</topic><topic>Medical sciences</topic><topic>Original</topic><topic>Pneumology</topic><topic>Radiation therapy and radiosensitizing agent</topic><topic>Radiation Tolerance - physiology</topic><topic>Transcriptional Activation</topic><topic>Treatment with physical agents</topic><topic>Treatment. General aspects</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>Tumors of the respiratory system and mediastinum</topic><topic>X-Rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Guanghui</creatorcontrib><creatorcontrib>Kong, Dejuan</creatorcontrib><creatorcontrib>Hou, Xue</creatorcontrib><creatorcontrib>Liang, Bing</creatorcontrib><creatorcontrib>He, Mengzi</creatorcontrib><creatorcontrib>Liang, Nan</creatorcontrib><creatorcontrib>Ma, Shumei</creatorcontrib><creatorcontrib>Liu, Xiaodong</creatorcontrib><collection>Pascal-Francis</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Public Health Database</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)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest 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>AIDS and Cancer Research Abstracts</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>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science 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>Cancer biotherapy & radiopharmaceuticals</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Guanghui</au><au>Kong, Dejuan</au><au>Hou, Xue</au><au>Liang, Bing</au><au>He, Mengzi</au><au>Liang, Nan</au><au>Ma, Shumei</au><au>Liu, Xiaodong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Tumor Suppressor, p53, Contributes to Radiosensitivity of Lung Cancer Cells by Regulating Autophagy and Apoptosis</atitle><jtitle>Cancer biotherapy & radiopharmaceuticals</jtitle><addtitle>Cancer Biother Radiopharm</addtitle><date>2013-03-01</date><risdate>2013</risdate><volume>28</volume><issue>2</issue><spage>153</spage><epage>159</epage><pages>153-159</pages><issn>1084-9785</issn><eissn>1557-8852</eissn><coden>CBRAFJ</coden><abstract>Cell death is one of the most important endpoints of radiosensitivity. The tumor suppressor p53 participates not only in regulation of apoptosis, but also in autophagy mechanism. In this study, H1299-P53 (with wild-type p53) and H1299-175H (with mutant 175H) were used, and the effects of p53 on radiosensitivity were analyzed.
Cell models with different p53 status were established by gene engineering, and cell viability was examined by colony formation assay, and cell counting kit-8 (CCK-8), 3-Methyladenine, and Z-VAD were used to block autophagy and apoptosis, respectively. Western blot was used to detect protein expression; monodansylcadaverine (MDC) staining was used to analyze autophagy rate; DAPI/Propidium Iodide (PI) staining and flow cytometry were used to assess apoptosis and necrosis.
In parental H1299, H1299-P53, and H1299-175H cells, radiosensitivity exhibited different by colony formation and CCK-8 assay (D0: 1.764 Gy, 1.407 Gy and 1.695 Gy; Dq: 2.977 Gy, 1.199 Gy and 2.312 Gy in turn). The radiosensitization of p53 was associated with the increase of MDM2 and P21 expression. The ionizing radiation (IR)-induced apoptosis was significant in H1299-P53 compared with in H1299 and H199-175H (p < 0.05) by flow cytometry, and the expression of cleaved-caspase3 was increased in H1299-P53 cells. While the IR-induced autophagy was significant in H1299 cells (p < 0.01) and decreased in H1299-P53 and H1299-175H cells (p < 0.01) by MDC staining, the expression of MAPLC3II and Beclin-1 increased in H1299, but not in H1299-p53 and H199-175H cells. The IR-induced cell survival was significantly increased by Z-VAD-FMK and decreased by 3MA in H1299-P53 cells; IR- induced autophagy was significantly increased by Z-VAD-FMK in H1299-P53 cells (p < 0.01), but not changed in H1299 cells.
p53 could regulate radiosensitivity by inhibiting autophagy and activating apoptosis; autophagy provides a prosurvival mechanism, and p53 potently abrogated the IR-induced autophagy, while mutant 175H shown no effect on radiosensitivity, suggesting that individual treatment strategies should be based on p53 status in patients.</abstract><cop>New Rochelle, NY</cop><pub>Liebert</pub><pmid>23268708</pmid><doi>10.1089/cbr.2012.1297</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer biotherapy & radiopharmaceuticals, 2013-03, Vol.28 (2), p.153-159 |
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| subjects | Apoptosis - radiation effects Autophagy - radiation effects Biological and medical sciences Blotting, Western Colony-Forming Units Assay Humans Lung cancer Lung Neoplasms - metabolism Lung Neoplasms - pathology Lung Neoplasms - radiotherapy Medical sciences Original Pneumology Radiation therapy and radiosensitizing agent Radiation Tolerance - physiology Transcriptional Activation Treatment with physical agents Treatment. General aspects Tumor Cells, Cultured Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors Tumors of the respiratory system and mediastinum X-Rays |
| title | The Tumor Suppressor, p53, Contributes to Radiosensitivity of Lung Cancer Cells by Regulating Autophagy and Apoptosis |
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