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<dc:title>TAp73 is one of the genes responsible for the lack of response to chemotherapy depending on B-Raf mutational status</dc:title>
<dc:creator>Herreros-Villanueva, Marta</dc:creator>
<dc:creator>Muñiz Rodríguez, Pilar</dc:creator>
<dc:creator>García Girón, Carlos</dc:creator>
<dc:creator>Cavia Saiz, Mónica</dc:creator>
<dc:creator>Coma del Corral, María J.</dc:creator>
<dc:subject>Salud</dc:subject>
<dc:subject>Biología molecular</dc:subject>
<dc:subject>Health</dc:subject>
<dc:subject>Molecular biology</dc:subject>
<dc:description>Background: Although there have been many studies on the p73 gene, some of its functions still remain unclear.&#xd;
There is little research on the relationship between p73 gene transcription and its protein expression and the&#xd;
response to certain drugs such as oxaliplatin and cetuximab, which are drugs currently used in colorectal cancer.&#xd;
The purpose of this study was to evaluate the impact of TAp73 expression on oxaliplatin and cetuximab-based&#xd;
chemotherapy in colorectal cancer cell lines with different K-Ras and B-Raf mutational status.&#xd;
Methods: TAp73 was analyzed in three colorectal tumor cell lines HT-29, SW-480 and Caco-2. mRNA TAp73 was&#xd;
determined using Real time PCR; TAp73 protein by immunoblotting and cell viability was analyzed by the MTT&#xd;
method.&#xd;
Results: We found that mRNA and TAp73 protein were decreased in cells treated with oxaliplatin (in monotherapy&#xd;
or combined with cetuximab) when B-Raf is mutated. This was statistically significant and was also associated with&#xd;
higher cell viability after the treatment.&#xd;
Conclusions: Here, for the first time we report, that there is a signaling loop between B-Raf activation and p73&#xd;
function.&#xd;
Low expression of TAp73 in colorectal cancer cell lines with mutated B-Raf may be involved in the lack of response&#xd;
to oxaliplatin in monotherapy or combined with cetuximab.</dc:description>
<dc:description>We thank B. De La Nogal and the Pharmacy Department for their generous help. Also, we thank CMV and her group in Leon. This work was supported by a grant FIS CA08/00070 from Instituto de Salud Carlos III, Spanish Ministerio de Ciencia e Innovación to MHV and Fundación Burgos por la Investigación de la Salud. MHV is especially thankful to CVP, IHH and AHV, for their support.</dc:description>
<dc:date>2023-11-21T08:59:34Z</dc:date>
<dc:date>2023-11-21T08:59:34Z</dc:date>
<dc:date>2010-02</dc:date>
<dc:type>info:eu-repo/semantics/article</dc:type>
<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
<dc:identifier>http://hdl.handle.net/10259/8072</dc:identifier>
<dc:identifier>10.1186/1479-5876-8-15</dc:identifier>
<dc:identifier>1479-5876</dc:identifier>
<dc:language>eng</dc:language>
<dc:relation>Journal of Translational Medicine. 2010, V. 8, n. 1</dc:relation>
<dc:relation>https://doi.org/10.1186/1479-5876-8-15</dc:relation>
<dc:rights>Attribution 3.0 Unported</dc:rights>
<dc:rights>http://creativecommons.org/licenses/by/3.0/</dc:rights>
<dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
<dc:format>application/pdf</dc:format>
<dc:publisher>Springer Nature</dc:publisher>
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