Subcellular Distribution of p53 by the p53-Responsive lncRNA NBAT1 Determines Chemotherapeutic Response in Neuroblastoma
Neuroblastoma has a low mutation rate for the gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation of wild-type p53. However, mechanisms leading to p53 inactivation via cytoplasmic accumulation are not well investigated. Here we sh...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2021-03, Vol.81 (6), p.1457-1471 |
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| creator | Mitra, Sanhita Muralidharan, Somsundar Veppil Di Marco, Mirco Juvvuna, Prasanna Kumar Kosalai, Subazini Thankaswamy Reischl, Silke Jachimowicz, Daniel Subhash, Santhilal Raimondi, Ivan Kurian, Leo Huarte, Maite Kogner, Per Fischer, Matthias Johnsen, John Inge Mondal, Tanmoy Kanduri, Chandrasekhar |
| description | Neuroblastoma has a low mutation rate for the
gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation of wild-type p53. However, mechanisms leading to p53 inactivation via cytoplasmic accumulation are not well investigated. Here we show that the neuroblastoma risk-associated locus 6p22.3-derived tumor suppressor
is a p53-responsive lncRNA that regulates p53 subcellular levels. Low expression of
provided resistance to genotoxic drugs by promoting p53 accumulation in cytoplasm and loss from mitochondrial and nuclear compartments. Depletion of
altered CRM1 function and contributed to the loss of p53-dependent nuclear gene expression during genotoxic drug treatment. CRM1 inhibition rescued p53-dependent nuclear functions and sensitized
-depleted cells to genotoxic drugs. Combined inhibition of CRM1 and MDM2 was even more effective in sensitizing aggressive neuroblastoma cells with p53 cytoplasmic accumulation. Thus, our mechanistic studies uncover an
-dependent CRM1/MDM2-based potential combination therapy for patients with high-risk neuroblastoma. SIGNIFICANCE: This study shows how a p53-responsive lncRNA mediates chemotherapeutic response by modulating nuclear p53 pathways and identifies a potential treatment strategy for patients with high-risk neuroblastoma. |
| doi_str_mv | 10.1158/0008-5472.CAN-19-3499 |
| format | Article |
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gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation of wild-type p53. However, mechanisms leading to p53 inactivation via cytoplasmic accumulation are not well investigated. Here we show that the neuroblastoma risk-associated locus 6p22.3-derived tumor suppressor
is a p53-responsive lncRNA that regulates p53 subcellular levels. Low expression of
provided resistance to genotoxic drugs by promoting p53 accumulation in cytoplasm and loss from mitochondrial and nuclear compartments. Depletion of
altered CRM1 function and contributed to the loss of p53-dependent nuclear gene expression during genotoxic drug treatment. CRM1 inhibition rescued p53-dependent nuclear functions and sensitized
-depleted cells to genotoxic drugs. Combined inhibition of CRM1 and MDM2 was even more effective in sensitizing aggressive neuroblastoma cells with p53 cytoplasmic accumulation. Thus, our mechanistic studies uncover an
-dependent CRM1/MDM2-based potential combination therapy for patients with high-risk neuroblastoma. SIGNIFICANCE: This study shows how a p53-responsive lncRNA mediates chemotherapeutic response by modulating nuclear p53 pathways and identifies a potential treatment strategy for patients with high-risk neuroblastoma.</description><identifier>ISSN: 0008-5472</identifier><identifier>ISSN: 1538-7445</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-19-3499</identifier><identifier>PMID: 33372039</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Apoptosis ; Cancer and Oncology ; Cancer och onkologi ; Cell and Molecular Biology ; Cell Fractionation ; Cell Line, Tumor ; Cell Nucleus - genetics ; Cell Nucleus - metabolism ; Cell- och molekylärbiologi ; Cytoplasm - genetics ; Cytoplasm - metabolism ; DNA Damage - drug effects ; Drug Resistance, Neoplasm - drug effects ; Drug Resistance, Neoplasm - genetics ; Exportin 1 Protein ; Farmaceutisk vetenskap ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Knockdown Techniques ; Humans ; Karyopherins - antagonists & inhibitors ; Karyopherins - metabolism ; Läkemedelskemi ; Male ; Medicin och hälsovetenskap ; Medicinal Chemistry ; Mice ; Mitochondria - genetics ; Mitochondria - metabolism ; Neuroblastoma - drug therapy ; Neuroblastoma - genetics ; Neuroblastoma - pathology ; Neuroblastoma - surgery ; Pharmaceutical Sciences ; Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors ; Proto-Oncogene Proteins c-mdm2 - metabolism ; Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors ; Receptors, Cytoplasmic and Nuclear - metabolism ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Xenograft Model Antitumor Assays</subject><ispartof>Cancer research (Chicago, Ill.), 2021-03, Vol.81 (6), p.1457-1471</ispartof><rights>2020 American Association for Cancer Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-68191fcf949b6c6d2576599afeaee5c290c09c14343ec2f644e6069e77ab17bc3</citedby><cites>FETCH-LOGICAL-c482t-68191fcf949b6c6d2576599afeaee5c290c09c14343ec2f644e6069e77ab17bc3</cites><orcidid>0000-0002-5563-2879 ; 0000-0002-0077-4597 ; 0000-0003-4296-9621 ; 0000-0003-1277-812X ; 0000-0002-2202-9694</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3356,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33372039$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/301006$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:146224412$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Mitra, Sanhita</creatorcontrib><creatorcontrib>Muralidharan, Somsundar Veppil</creatorcontrib><creatorcontrib>Di Marco, Mirco</creatorcontrib><creatorcontrib>Juvvuna, Prasanna Kumar</creatorcontrib><creatorcontrib>Kosalai, Subazini Thankaswamy</creatorcontrib><creatorcontrib>Reischl, Silke</creatorcontrib><creatorcontrib>Jachimowicz, Daniel</creatorcontrib><creatorcontrib>Subhash, Santhilal</creatorcontrib><creatorcontrib>Raimondi, Ivan</creatorcontrib><creatorcontrib>Kurian, Leo</creatorcontrib><creatorcontrib>Huarte, Maite</creatorcontrib><creatorcontrib>Kogner, Per</creatorcontrib><creatorcontrib>Fischer, Matthias</creatorcontrib><creatorcontrib>Johnsen, John Inge</creatorcontrib><creatorcontrib>Mondal, Tanmoy</creatorcontrib><creatorcontrib>Kanduri, Chandrasekhar</creatorcontrib><title>Subcellular Distribution of p53 by the p53-Responsive lncRNA NBAT1 Determines Chemotherapeutic Response in Neuroblastoma</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Neuroblastoma has a low mutation rate for the
gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation of wild-type p53. However, mechanisms leading to p53 inactivation via cytoplasmic accumulation are not well investigated. Here we show that the neuroblastoma risk-associated locus 6p22.3-derived tumor suppressor
is a p53-responsive lncRNA that regulates p53 subcellular levels. Low expression of
provided resistance to genotoxic drugs by promoting p53 accumulation in cytoplasm and loss from mitochondrial and nuclear compartments. Depletion of
altered CRM1 function and contributed to the loss of p53-dependent nuclear gene expression during genotoxic drug treatment. CRM1 inhibition rescued p53-dependent nuclear functions and sensitized
-depleted cells to genotoxic drugs. Combined inhibition of CRM1 and MDM2 was even more effective in sensitizing aggressive neuroblastoma cells with p53 cytoplasmic accumulation. Thus, our mechanistic studies uncover an
-dependent CRM1/MDM2-based potential combination therapy for patients with high-risk neuroblastoma. SIGNIFICANCE: This study shows how a p53-responsive lncRNA mediates chemotherapeutic response by modulating nuclear p53 pathways and identifies a potential treatment strategy for patients with high-risk neuroblastoma.</description><subject>Animals</subject><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Apoptosis</subject><subject>Cancer and Oncology</subject><subject>Cancer och onkologi</subject><subject>Cell and Molecular Biology</subject><subject>Cell Fractionation</subject><subject>Cell Line, Tumor</subject><subject>Cell Nucleus - genetics</subject><subject>Cell Nucleus - metabolism</subject><subject>Cell- och molekylärbiologi</subject><subject>Cytoplasm - genetics</subject><subject>Cytoplasm - metabolism</subject><subject>DNA Damage - drug effects</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Exportin 1 Protein</subject><subject>Farmaceutisk vetenskap</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>Karyopherins - antagonists & inhibitors</subject><subject>Karyopherins - metabolism</subject><subject>Läkemedelskemi</subject><subject>Male</subject><subject>Medicin och hälsovetenskap</subject><subject>Medicinal Chemistry</subject><subject>Mice</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>Neuroblastoma - drug therapy</subject><subject>Neuroblastoma - genetics</subject><subject>Neuroblastoma - pathology</subject><subject>Neuroblastoma - surgery</subject><subject>Pharmaceutical Sciences</subject><subject>Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-mdm2 - metabolism</subject><subject>Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0008-5472</issn><issn>1538-7445</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kctO3DAUhq0KVKa0j9DKL-Cp74mXw0ChEppKQNeW4zmB0CSO7ITL29fRDMOqXZ2L_u-cxYfQV0aXjKnyO6W0JEoWfLlebQgzREhjPqAFU6IkhZTqCC0OmRP0KaXHPCpG1Ud0IoQoOBVmgV5up8pD206ti_i8SWNsqmlsQo9DjQclcPWKxweYW3IDaQh9ap4At72_2azw5mx1x_A5jBC7poeE1w_QhZyPboB8xuM9A7jp8QamGKrWpTF07jM6rl2b4Mu-nqLfPy7u1lfk-tflz_XqmnhZ8pHokhlW-9pIU2mvt1wVWhnjanAAynNDPTWeSSEFeF5rKUFTbaAoXMWKyotTRHZ30zMMU2WH2HQuvtrgGrtf_ckdWKmVUjLnzT_zQwzbd-gNZFJzLiXj__11Pw02r-6nGRGUUapzXu3yPoaUItQHglE7W7azQTsbtNmyZcbOljP3bcflJx1sD9SbVvEXCVOmDA</recordid><startdate>20210315</startdate><enddate>20210315</enddate><creator>Mitra, Sanhita</creator><creator>Muralidharan, Somsundar Veppil</creator><creator>Di Marco, Mirco</creator><creator>Juvvuna, Prasanna Kumar</creator><creator>Kosalai, Subazini Thankaswamy</creator><creator>Reischl, Silke</creator><creator>Jachimowicz, Daniel</creator><creator>Subhash, Santhilal</creator><creator>Raimondi, Ivan</creator><creator>Kurian, Leo</creator><creator>Huarte, Maite</creator><creator>Kogner, Per</creator><creator>Fischer, Matthias</creator><creator>Johnsen, John Inge</creator><creator>Mondal, Tanmoy</creator><creator>Kanduri, Chandrasekhar</creator><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>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope><orcidid>https://orcid.org/0000-0002-5563-2879</orcidid><orcidid>https://orcid.org/0000-0002-0077-4597</orcidid><orcidid>https://orcid.org/0000-0003-4296-9621</orcidid><orcidid>https://orcid.org/0000-0003-1277-812X</orcidid><orcidid>https://orcid.org/0000-0002-2202-9694</orcidid></search><sort><creationdate>20210315</creationdate><title>Subcellular Distribution of p53 by the p53-Responsive lncRNA NBAT1 Determines Chemotherapeutic Response in Neuroblastoma</title><author>Mitra, Sanhita ; Muralidharan, Somsundar Veppil ; Di Marco, Mirco ; Juvvuna, Prasanna Kumar ; Kosalai, Subazini Thankaswamy ; Reischl, Silke ; Jachimowicz, Daniel ; Subhash, Santhilal ; Raimondi, Ivan ; Kurian, Leo ; Huarte, Maite ; Kogner, Per ; Fischer, Matthias ; Johnsen, John Inge ; Mondal, Tanmoy ; Kanduri, Chandrasekhar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-68191fcf949b6c6d2576599afeaee5c290c09c14343ec2f644e6069e77ab17bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antineoplastic Combined Chemotherapy Protocols - pharmacology</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Apoptosis</topic><topic>Cancer and Oncology</topic><topic>Cancer och onkologi</topic><topic>Cell and Molecular Biology</topic><topic>Cell Fractionation</topic><topic>Cell Line, Tumor</topic><topic>Cell Nucleus - genetics</topic><topic>Cell Nucleus - metabolism</topic><topic>Cell- och molekylärbiologi</topic><topic>Cytoplasm - genetics</topic><topic>Cytoplasm - metabolism</topic><topic>DNA Damage - drug effects</topic><topic>Drug Resistance, Neoplasm - drug effects</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Exportin 1 Protein</topic><topic>Farmaceutisk vetenskap</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Karyopherins - antagonists & inhibitors</topic><topic>Karyopherins - metabolism</topic><topic>Läkemedelskemi</topic><topic>Male</topic><topic>Medicin och hälsovetenskap</topic><topic>Medicinal Chemistry</topic><topic>Mice</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - metabolism</topic><topic>Neuroblastoma - drug therapy</topic><topic>Neuroblastoma - genetics</topic><topic>Neuroblastoma - pathology</topic><topic>Neuroblastoma - surgery</topic><topic>Pharmaceutical Sciences</topic><topic>Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors</topic><topic>Proto-Oncogene Proteins c-mdm2 - metabolism</topic><topic>Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors</topic><topic>Receptors, Cytoplasmic and Nuclear - metabolism</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mitra, Sanhita</creatorcontrib><creatorcontrib>Muralidharan, Somsundar Veppil</creatorcontrib><creatorcontrib>Di Marco, Mirco</creatorcontrib><creatorcontrib>Juvvuna, Prasanna Kumar</creatorcontrib><creatorcontrib>Kosalai, Subazini Thankaswamy</creatorcontrib><creatorcontrib>Reischl, Silke</creatorcontrib><creatorcontrib>Jachimowicz, Daniel</creatorcontrib><creatorcontrib>Subhash, Santhilal</creatorcontrib><creatorcontrib>Raimondi, Ivan</creatorcontrib><creatorcontrib>Kurian, Leo</creatorcontrib><creatorcontrib>Huarte, Maite</creatorcontrib><creatorcontrib>Kogner, Per</creatorcontrib><creatorcontrib>Fischer, Matthias</creatorcontrib><creatorcontrib>Johnsen, John Inge</creatorcontrib><creatorcontrib>Mondal, Tanmoy</creatorcontrib><creatorcontrib>Kanduri, Chandrasekhar</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mitra, Sanhita</au><au>Muralidharan, Somsundar Veppil</au><au>Di Marco, Mirco</au><au>Juvvuna, Prasanna Kumar</au><au>Kosalai, Subazini Thankaswamy</au><au>Reischl, Silke</au><au>Jachimowicz, Daniel</au><au>Subhash, Santhilal</au><au>Raimondi, Ivan</au><au>Kurian, Leo</au><au>Huarte, Maite</au><au>Kogner, Per</au><au>Fischer, Matthias</au><au>Johnsen, John Inge</au><au>Mondal, Tanmoy</au><au>Kanduri, Chandrasekhar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Subcellular Distribution of p53 by the p53-Responsive lncRNA NBAT1 Determines Chemotherapeutic Response in Neuroblastoma</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2021-03-15</date><risdate>2021</risdate><volume>81</volume><issue>6</issue><spage>1457</spage><epage>1471</epage><pages>1457-1471</pages><issn>0008-5472</issn><issn>1538-7445</issn><eissn>1538-7445</eissn><abstract>Neuroblastoma has a low mutation rate for the
gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation of wild-type p53. However, mechanisms leading to p53 inactivation via cytoplasmic accumulation are not well investigated. Here we show that the neuroblastoma risk-associated locus 6p22.3-derived tumor suppressor
is a p53-responsive lncRNA that regulates p53 subcellular levels. Low expression of
provided resistance to genotoxic drugs by promoting p53 accumulation in cytoplasm and loss from mitochondrial and nuclear compartments. Depletion of
altered CRM1 function and contributed to the loss of p53-dependent nuclear gene expression during genotoxic drug treatment. CRM1 inhibition rescued p53-dependent nuclear functions and sensitized
-depleted cells to genotoxic drugs. Combined inhibition of CRM1 and MDM2 was even more effective in sensitizing aggressive neuroblastoma cells with p53 cytoplasmic accumulation. Thus, our mechanistic studies uncover an
-dependent CRM1/MDM2-based potential combination therapy for patients with high-risk neuroblastoma. SIGNIFICANCE: This study shows how a p53-responsive lncRNA mediates chemotherapeutic response by modulating nuclear p53 pathways and identifies a potential treatment strategy for patients with high-risk neuroblastoma.</abstract><cop>United States</cop><pmid>33372039</pmid><doi>10.1158/0008-5472.CAN-19-3499</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-5563-2879</orcidid><orcidid>https://orcid.org/0000-0002-0077-4597</orcidid><orcidid>https://orcid.org/0000-0003-4296-9621</orcidid><orcidid>https://orcid.org/0000-0003-1277-812X</orcidid><orcidid>https://orcid.org/0000-0002-2202-9694</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0008-5472 |
| ispartof | Cancer research (Chicago, Ill.), 2021-03, Vol.81 (6), p.1457-1471 |
| issn | 0008-5472 1538-7445 1538-7445 |
| language | eng |
| recordid | cdi_swepub_primary_oai_swepub_ki_se_465554 |
| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Antineoplastic Combined Chemotherapy Protocols - pharmacology Antineoplastic Combined Chemotherapy Protocols - therapeutic use Apoptosis Cancer and Oncology Cancer och onkologi Cell and Molecular Biology Cell Fractionation Cell Line, Tumor Cell Nucleus - genetics Cell Nucleus - metabolism Cell- och molekylärbiologi Cytoplasm - genetics Cytoplasm - metabolism DNA Damage - drug effects Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics Exportin 1 Protein Farmaceutisk vetenskap Female Gene Expression Regulation, Neoplastic - drug effects Gene Knockdown Techniques Humans Karyopherins - antagonists & inhibitors Karyopherins - metabolism Läkemedelskemi Male Medicin och hälsovetenskap Medicinal Chemistry Mice Mitochondria - genetics Mitochondria - metabolism Neuroblastoma - drug therapy Neuroblastoma - genetics Neuroblastoma - pathology Neuroblastoma - surgery Pharmaceutical Sciences Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors Proto-Oncogene Proteins c-mdm2 - metabolism Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors Receptors, Cytoplasmic and Nuclear - metabolism RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Xenograft Model Antitumor Assays |
| title | Subcellular Distribution of p53 by the p53-Responsive lncRNA NBAT1 Determines Chemotherapeutic Response in Neuroblastoma |
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