<?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>0535-5133</journal-id>
<journal-title><![CDATA[Investigación Clínica]]></journal-title>
<abbrev-journal-title><![CDATA[Invest. clín]]></abbrev-journal-title>
<issn>0535-5133</issn>
<publisher>
<publisher-name><![CDATA[Instituto de Investigaciones Clínicas "Dr. Américo Negrette", Facultad de Medicina, Universidad del Zulia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0535-51332024000300267</article-id>
<article-id pub-id-type="doi">10.54817/ic.v65n3a01</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Dihydroartemisinin, an artemisinin derivative, reverses oxaliplatin resistance in human colorectal cancer cells by regulating the SIRT3/PI3K/AKT signalling pathway.]]></article-title>
<article-title xml:lang="es"><![CDATA[La dihidroartemisinina, un derivado de la artemisinina, revierte la resistencia al oxaliplatino en células humanas de cáncer colorrectal mediante la regulación de la vía de señalización SIRT3/PI3K/AKT.]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Shen]]></surname>
<given-names><![CDATA[Xiaodong]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Shi]]></surname>
<given-names><![CDATA[Chencheng]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Lei]]></surname>
<given-names><![CDATA[Ming]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Zhou]]></surname>
<given-names><![CDATA[Rongjian]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Liu]]></surname>
<given-names><![CDATA[Shaoqun]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Su]]></surname>
<given-names><![CDATA[Chang]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Fudan University Minhang Hospital Department of Gastrointestinal Surgery]]></institution>
<addr-line><![CDATA[Shanghai ]]></addr-line>
<country>China</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2024</year>
</pub-date>
<volume>65</volume>
<numero>3</numero>
<fpage>267</fpage>
<lpage>278</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_arttext&amp;pid=S0535-51332024000300267&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_abstract&amp;pid=S0535-51332024000300267&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_pdf&amp;pid=S0535-51332024000300267&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Dihydroartemisinin (DHA), a derivative of artemisinin, has been shown to act as a chemosensitizer of various cancer chemotherapeutic agents both in vitro and in vivo. However, in colorectal cancer (CRC), no study has focused on the effect of DHA on oxaliplatin (L -OHP) resistance. Our study aimed to examine the effectiveness of DHA in reversing the resistance of human CRC cells to L -OHP, as well as its underlying molecular mechanisms. LoVo cells were purchased from ATCC, while LoVo/L -OHP cells were obtained by exposing LoVo cells to progressively increasing concentrations of L -OHP. LoVo/L -OHP were treated with various concentrations of DHA, and cell apoptosis ratio and viability were assessed by flow cytometry and CCK-8. Our results showed that DHA treatment remarkably decreased the viability of LoVo/L -OHP cells and increased the apoptosis ratio. As the mechanism of action, we found that DHA enhanced the expression of Sirtuin 3 (SIRT3) and suppressed the phosphatidylinositol 3-kinase (PI3K)/AKT signalling cascade. Silencing of SIRT3 reversed the effect of DHA on cell apoptosis and viability by activating the PI3K/AKT axis in LoVo/L -OHP cells. Overall, our study found that DHA has the ability to counteract L -OHP resistance in LoVo/L -OHP cells through the modulation of the SIRT3/PI3K/AKT signalling pathway, suggesting a new research target for CRC treatment.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen Se ha demostrado que la dihidroartemisinina (DHA), un derivado de la artemisinina, actúa como quimiosensibilizador de diversos agentes quimioterapéuticos contra el cáncer tanto in vitro como in vivo. Sin embargo, en el cáncer colorrectal (CCR), ningún estudio se ha centrado en el efecto del DHA sobre la resistencia al oxaliplatino (L -OHP). El objetivo de nuestro estudio era examinar la eficacia del DHA para revertir la resistencia de las células humanas de CCR al L -OHP, así como sus mecanismos moleculares subyacentes. Las células LoVo se adquirieron a ATCC, mientras que las células LoVo/L -OHP se obtuvieron exponiendo las células LoVo a concentraciones progresivamente crecientes de L -OHP. Las células LoVo/L -OHP se trataron con diversas concentraciones de DHA, y el índice de apoptosis celular y la viabilidad se evaluaron mediante citometría de flujo y CCK-8. Nuestros resultados mostraron que el tratamiento con DHA disminuía notablemente la viabilidad de las células LoVo/L -OHP y aumentaba el índice de apoptosis. Desde el punto de vista de su mecanismo de acción, se observó que el DHA potenciaba la expresión de la sirtuina 3 (SIRT3) y suprimía la cascada de señalización fosfatidilinositol 3-cinasa (PI3K)/AKT. El silenciamiento de SIRT3 revirtió el efecto del DHA sobre la apoptosis y la viabilidad celular a través de la activación del eje PI3K/AKT en las células LoVo/L -OHP. En conjunto, nuestro estudio descubrió la capacidad del DHA para contrarrestar la resistencia a L -OHP en células LoVo/L -OHP a través de la modulación de la vía de señalización SIRT3/PI3K/AKT, lo cual sugiere una nueva foco de investigación para el tratamiento del CCR.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[dihydroartemisinin]]></kwd>
<kwd lng="en"><![CDATA[SIRT3]]></kwd>
<kwd lng="en"><![CDATA[oxaliplatin]]></kwd>
<kwd lng="en"><![CDATA[colorectal cancer]]></kwd>
<kwd lng="es"><![CDATA[dihidroartemisinina]]></kwd>
<kwd lng="es"><![CDATA[SIRT3]]></kwd>
<kwd lng="es"><![CDATA[oxaliplatino]]></kwd>
<kwd lng="es"><![CDATA[cáncer colorrectal]]></kwd>
</kwd-group>
</article-meta>
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