<?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>S0535-51332026000100073</article-id>
<article-id pub-id-type="doi">10.54817/ic.v67n1a06</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Withaferin-A induces apoptosis and autophagy in colorectal cancer cell lines via down-regulated expression of histone deacetylase 1.]]></article-title>
<article-title xml:lang="es"><![CDATA[La withaferina-A induce la apoptosis y la autofagia en líneas celulares de cáncer colorrectal mediante la regulación negativa de la expresión de la histona deacetilasa 1.]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Wang]]></surname>
<given-names><![CDATA[Qiong]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Li]]></surname>
<given-names><![CDATA[Caixia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Qilu Hospital of Shandong University  ]]></institution>
<addr-line><![CDATA[Jinan Shandong]]></addr-line>
<country>China</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Weifang NO.2 People's Hospital Endoscopy Center ]]></institution>
<addr-line><![CDATA[Weifang Shandong]]></addr-line>
<country>China</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Shandong Provincial People&#8217;s Hospital Department of Stomatology ]]></institution>
<addr-line><![CDATA[Jinan Shandong]]></addr-line>
<country>China</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2026</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2026</year>
</pub-date>
<volume>67</volume>
<numero>1</numero>
<fpage>73</fpage>
<lpage>91</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_arttext&amp;pid=S0535-51332026000100073&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_abstract&amp;pid=S0535-51332026000100073&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_pdf&amp;pid=S0535-51332026000100073&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Colorectal cancer (CRC) remains the third most common malignancy worldwide, and there is an urgent need for low-toxicity, mechanism-based preventives or adjuvants. Withaferin-A (WA), a plant-derived steroidal lactone, exhibits broad antitumor activity; however, its role in CRC and its interactions with epigenetic regulators, such as histone deacetylase 1 (HDAC1), remain unclear. Therefore, we investigated whether WA suppresses CRC growth by down-regulating HDAC1 while inducing apoptosis and autophagy. Caco2 and HT-29 cells were treated with 0-5 µM WA; viability, colony formation, and migration decreased significantly (IC50 0.70-1.52 µM). Techniques such as Annexin-V/7-AAD flow cytometry, MDC staining, TEM, and LC3B immunofluorescence showed that 1 µM WA notably increased apoptosis and autophagic flux, along with reduced HDAC1 and p62 levels, higher LC3B-II/I ratios, and an increased Bax/Bcl-2 ratio. Overexpression of HDAC1 via a lentiviral vector reversed these effects, confirming dependence on HDAC1. For translational relevance, eight-week-old C57BL/6J mice were first exposed to the food-borne carcinogen IQ (2-amino-3-methyl-3H-imidazo[4,5-f]quinoline, 100 mg/kg) every other day for three weeks to induce aberrant crypt foci (ACF). Starting the day after the first IQ dose, animals received WA (2 mg/kg) or vehicle (corn oil) by gavage every other day for the same period. WA reduced the number of macroscopic ACF by more than 60%, restored HDAC1-related LC3B and p62 expression to normal levels, and showed no toxicity based on body weight or general health assessments. These findings suggest that WA provides potent, low-toxicity chemopreventive effects against CRC lesion formation through HDAC1-dependent induction of apoptosis and autophagy, supporting its further consideration as a preventive or adjuvant agent.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen El cáncer colorrectal (CCR) sigue siendo la tercera malignidad más común en todo el mundo, y existe una necesidad urgente de preventivos o adyuvantes de baja toxicidad basados en mecanismos. Withaferin-A (WA), una lactona esteroide derivada de plantas, ha mostrado una amplia actividad antitumoral, pero su papel en el CRC y su interacción con reguladores epigenéticos, como la histona deacetilasa 1 (HDAC1), no están claros. Por lo tanto, se evaluó si WA suprime el crecimiento de CRC al regular la actividad de HDAC1 hacia abajo e inducir concomitantemente apoptosis y autofagia. Las células Caco2 y HT-29 se expusieron a WA 0-5 µM; la viabilidad, la formación de colonias y la migración se inhibieron marcadamente (IC50 0.70-1.52 µM). La citometría de flujo con Annexin-V/7-AAD, la tinción con MDC, la inmunofluorescencia de TEM y de LC3B mostraron que WA a 1 µM aumentó significativamente la apoptosis y el flujo autofágico, acompañados de la regulación descendente de HDAC1 y p62, la regulación ascendente de LC3B-II/I y un aumento en la relación Bax/ Bcl-2. La sobreexpresión de HDAC1 mediada por lentivirus revertió todos estos efectos, lo que confirma la dependencia de HDAC1. Para evaluar la relevancia traslacional, a ratones C57BL/6J de ocho semanas de edad se les administró primero el carcinógeno el carcinógeno de origen alimentario, 2-amino, 2-amino-3-metil-3H-imidazo[4,5-f]quinoline (100 mg/kg), cada dos días durante 3 semanas, para inducir focos de cripta aberrantes (ACF). A partir del día siguiente a la primera dosis de carcinógeno, los animales recibieron, adicionalmente, WA (2 mg/kg) o vehículo (aceite de maíz) por gavage cada dos días durante el mismo período. WA redujo el número macroscópico de ACF en más del 60%, restableció la expresión de LC3B y p62 asociada a HDAC1 a niveles normales y no mostró toxicidad ni en el peso corporal ni en el monitoreo general de la salud. Estos datos indican que WA ejerce una quimioprevención potente y de baja toxicidad contra la formación de lesiones de CRC mediante la inducción de apoptosis y autofagia dependientes de HDAC1, lo que respalda su desarrollo adicional como agente preventivo o adyuvante.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Apoptosis]]></kwd>
<kwd lng="en"><![CDATA[Autophagy]]></kwd>
<kwd lng="en"><![CDATA[Histone Deacetylase 1]]></kwd>
<kwd lng="en"><![CDATA[Aberrant Crypt Foci]]></kwd>
<kwd lng="en"><![CDATA[Chemoprevention]]></kwd>
<kwd lng="es"><![CDATA[Apoptosis]]></kwd>
<kwd lng="es"><![CDATA[Autofagia]]></kwd>
<kwd lng="es"><![CDATA[Histona Desacetilasa 1]]></kwd>
<kwd lng="es"><![CDATA[Focos de Criptas Aberrantes]]></kwd>
<kwd lng="es"><![CDATA[Quimioprevención]]></kwd>
</kwd-group>
</article-meta>
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