<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>2007-7858</journal-id>
<journal-title><![CDATA[CienciaUAT]]></journal-title>
<abbrev-journal-title><![CDATA[CienciaUAT]]></abbrev-journal-title>
<issn>2007-7858</issn>
<publisher>
<publisher-name><![CDATA[Universidad Autónoma de Tamaulipas]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2007-78582025000100063</article-id>
<article-id pub-id-type="doi">10.29059/cienciauat.v19i2.1917</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Transportadores de Ca2+ y su papel en las características distintivas del cáncer]]></article-title>
<article-title xml:lang="en"><![CDATA[Ca2+ Transporters and Their Role in the Cancer Hallmarks]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Monge-Hernández]]></surname>
<given-names><![CDATA[Indra Nicole]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Santiago-García]]></surname>
<given-names><![CDATA[Juan]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Veracruzana Instituto de Investigaciones Biológicas Laboratorio de Biología Molecular]]></institution>
<addr-line><![CDATA[Xalapa Veracruz]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>06</month>
<year>2025</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>06</month>
<year>2025</year>
</pub-date>
<volume>19</volume>
<numero>2</numero>
<fpage>63</fpage>
<lpage>77</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S2007-78582025000100063&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S2007-78582025000100063&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S2007-78582025000100063&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen El ion calcio (Ca2+) activa diversas vías de señalización importantes en diferentes procesos celulares como proliferación, progresión del ciclo celular, apoptosis y expresión génica. La homeostasis de Ca2+ depende de diversas proteínas, que actúan como canales, bombas, receptores, sitios de unión y almacenamiento de Ca2+, las cuales son de gran importancia porque regulan el flujo, compartimentación y concentración del Ca2+ celular, para que las vías de señalización dependientes de este catión funcionen adecuadamente. El objetivo del presente trabajo fue analizar la información existente sobre los cambios en la expresión de transportadores de Ca2+ en cáncer y su participación en las características distintivas de la enfermedad, principalmente la proliferación celular descontrolada, la resistencia a la apoptosis o la activación de la migración e invasión celular. La evidencia indica que múltiples canales de Ca2+ se sobreexpresan en cáncer, lo que se asocia con incremento del Ca2+ citoplásmico y activación de las vías de señalización CaM/CaN/NFAT, Akt o MAPK/ERK, situación que puede conducir a un incremento en la proliferación, transición epitelio-mesenquimal, mayor capacidad de migración e invasión celular. Por otro lado, la subexpresión de bombas de Ca2+ o sobreexpresión de canales mitocondriales contribuye a la evasión de la apoptosis, a la par que propicia la migración celular. El estudio de transportadores de Ca2+ con expresión alterada en cáncer puede contribuir a la identificación de potenciales biomarcadores o blancos terapéuticos que permitan el desarrollo de nuevas terapias.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Calcium ion (Ca2+) activates crucial signaling pathways involved in different cellular processes, such as proliferation, cell cycle progression, apoptosis and gene expression. Ca2+ signaling depends on various proteins, including channels, pumps, receptors, and binding or storage proteins, which regulate Ca2+ influx, compartmentalization, and concentration for Ca2+ dependent signaling pathways to function properly. This work aimed to analyze evidence regarding the altered expression of Ca2+ transporters in cancer and their contribution to the hallmarks of the disease, mainly sustained cellular proliferation, apoptosis resistance, and activation of migration and invasion. Evidence suggests that overexpression of Ca2+ channels in cancer is associated with increased Ca2+ entry and activation of CaM/CaN/NFAT, Akt or MAPK/ERK signaling pathways, leading to cell proliferation, migration, invasion, and epithelial-mesenchymal transition. On the other hand, the downregulation of Ca2+ pumps or upregulation of mitochondrial channels contributes to apoptosis evasion and enhanced cellular migration. Research on Ca2+ transporters with deregulated expression in cancer may contribute to the identification of potential biomarkers and therapeutic targets for the development of new treatments.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[cáncer]]></kwd>
<kwd lng="es"><![CDATA[transportadores de calcio]]></kwd>
<kwd lng="es"><![CDATA[proliferación celular]]></kwd>
<kwd lng="es"><![CDATA[apoptosis]]></kwd>
<kwd lng="es"><![CDATA[migración e invasión celular]]></kwd>
<kwd lng="en"><![CDATA[cancer]]></kwd>
<kwd lng="en"><![CDATA[calcium transporters]]></kwd>
<kwd lng="en"><![CDATA[cell proliferation]]></kwd>
<kwd lng="en"><![CDATA[apoptosis]]></kwd>
<kwd lng="en"><![CDATA[cell migration and invasion]]></kwd>
</kwd-group>
</article-meta>
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