دورية أكاديمية
أعرض في EDS

HOTAIR Promotes the Hyperactivation of PI3K/Akt and Wnt/β-Catenin Signaling Pathways via PTEN Hypermethylation in Cervical Cancer.

التفاصيل البيبلوغرافية
العنوان: HOTAIR Promotes the Hyperactivation of PI3K/Akt and Wnt/β-Catenin Signaling Pathways via PTEN Hypermethylation in Cervical Cancer.
المؤلفون: Trujano-Camacho S; Experimental Biology PhD Program, DCBS, Universidad Autónoma Metropolitana-Iztapalapa, Mexico City 09340, Mexico.; Laboratorio de Genómica, Instituto Nacional de Cancerología, Av. San Fernando 22, Belisario Domínguez Secc 16, Tlalpan, Ciudad de México 14080, Mexico., Cantú-de León D; Laboratorio de Genómica, Instituto Nacional de Cancerología, Av. San Fernando 22, Belisario Domínguez Secc 16, Tlalpan, Ciudad de México 14080, Mexico., Pérez-Yepez E; Laboratorio de Genómica, Instituto Nacional de Cancerología, Av. San Fernando 22, Belisario Domínguez Secc 16, Tlalpan, Ciudad de México 14080, Mexico., Contreras-Romero C; Laboratorio de Genómica, Instituto Nacional de Cancerología, Av. San Fernando 22, Belisario Domínguez Secc 16, Tlalpan, Ciudad de México 14080, Mexico., Coronel-Hernandez J; Laboratorio de Genómica, Instituto Nacional de Cancerología, Av. San Fernando 22, Belisario Domínguez Secc 16, Tlalpan, Ciudad de México 14080, Mexico., Millan-Catalan O; Laboratorio de Genómica, Instituto Nacional de Cancerología, Av. San Fernando 22, Belisario Domínguez Secc 16, Tlalpan, Ciudad de México 14080, Mexico., Rodríguez-Dorantes M; Laboratorio de Oncogenómica, Instituto Nacional de Medicina Genómica (INMEGEN), Mexico City 14610, Mexico., López-Camarillo C; Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México 03100, Mexico., Gutiérrez-Ruiz C; Laboratory of Experimental Medicine, Translational Medicine Unit, Instituto de Investigaciones Biomédicas, UNAM/Instituto Nacional de Cardiología Ignacio Chávez, Tlalpan, Mexico City 14080, Mexico.; Department of Health Sciences, Universidad Autónoma Metropolitana-Iztapalapa, Mexico City 09340, Mexico., Jacobo-Herrera N; Unidad de Bioquímica, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubiran, Av. Vasco de Quiroga 15, Col. Belisario Domínguez Sección XVI, Tlalpan, Ciudad de México 14080, Mexico., Pérez-Plasencia C; Laboratorio de Genómica, Instituto Nacional de Cancerología, Av. San Fernando 22, Belisario Domínguez Secc 16, Tlalpan, Ciudad de México 14080, Mexico.; Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla 54090, Mexico.
المصدر: Cells [Cells] 2024 Sep 04; Vol. 13 (17). Date of Electronic Publication: 2024 Sep 04.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: Uterine Cervical Neoplasms*/genetics , Uterine Cervical Neoplasms*/metabolism , Uterine Cervical Neoplasms*/pathology , Proto-Oncogene Proteins c-akt*/metabolism , RNA, Long Noncoding*/genetics , RNA, Long Noncoding*/metabolism , PTEN Phosphohydrolase*/metabolism , PTEN Phosphohydrolase*/genetics , Phosphatidylinositol 3-Kinases*/metabolism , Wnt Signaling Pathway*/genetics , DNA Methylation*/genetics , Hypoxia-Inducible Factor 1, alpha Subunit*/metabolism , Hypoxia-Inducible Factor 1, alpha Subunit*/genetics, Humans ; Female ; HeLa Cells ; Gene Expression Regulation, Neoplastic ; beta Catenin/metabolism ; beta Catenin/genetics ; Promoter Regions, Genetic/genetics ; DNA (Cytosine-5-)-Methyltransferase 1/metabolism ; DNA (Cytosine-5-)-Methyltransferase 1/genetics
مستخلص: The mechanisms underlying the sustained activation of the PI3K/AKT and Wnt/β-catenin pathways mediated by HOTAIR in cervical cancer (CC) have not been extensively described. To address this knowledge gap in the literature, we explored the interactions between these pathways by driving HOTAIR expression levels in HeLa cells. Our findings reveal that HOTAIR is a key regulator in sustaining the activation of both signaling pathways. Specifically, altering HOTAIR expression-either by knockdown or overexpression-significantly influenced the transcriptional activity of the PI3K/AKT and Wnt/β-catenin pathways. Additionally, we discovered that HIF1α directly induces HOTAIR transcription, which in turn leads to the epigenetic silencing of the PTEN promoter via DNMT1. This process leads to the sustained activation of both pathways, highlighting a novel regulatory axis involving HOTAIR and HIF1α in cervical cancer. Our results suggest a new model in which HOTAIR sustains reciprocal activation of the PI3K/AKT and Wnt/β-catenin pathways through the HOTAIR/HIF1α axis, thereby contributing to the oncogenic phenotype of cervical cancer.
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فهرسة مساهمة: Keywords: HOTAIR; LncRNAs; PI3K/AKT pathway; Wntl/β-catenin pathway; epigenetic regulation
المشرفين على المادة: 0 (HOTAIR long untranslated RNA, human)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
0 (RNA, Long Noncoding)
EC 3.1.3.67 (PTEN Phosphohydrolase)
EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
0 (Hypoxia-Inducible Factor 1, alpha Subunit)
EC 3.1.3.67 (PTEN protein, human)
0 (beta Catenin)
EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1)
تواريخ الأحداث: Date Created: 20240914 Date Completed: 20240914 Latest Revision: 20240916
رمز التحديث: 20240916
مُعرف محوري في PubMed: PMC11394386
DOI: 10.3390/cells13171484
PMID: 39273054
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4409
DOI:10.3390/cells13171484