دورية أكاديمية
أعرض في EDS

Ibrutinib Modulates Proliferation, Migration, Mitochondrial Homeostasis, and Apoptosis in Melanoma Cells.

التفاصيل البيبلوغرافية
العنوان: Ibrutinib Modulates Proliferation, Migration, Mitochondrial Homeostasis, and Apoptosis in Melanoma Cells.
المؤلفون: Lins FV; Laboratório de Hematologia e Células-Tronco, Faculdade de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, DF, Brazil.; Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Bispo ECI; Laboratório de Hematologia e Células-Tronco, Faculdade de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, DF, Brazil., Rodrigues NS; Laboratório de Hematologia e Células-Tronco, Faculdade de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, DF, Brazil., Silva MVS; Laboratório Interdisciplinar de Biociências, Faculdade de Medicina, Universidade de Brasília, Brasília 70910-900, DF, Brazil., Carvalho JL; Laboratório Interdisciplinar de Biociências, Faculdade de Medicina, Universidade de Brasília, Brasília 70910-900, DF, Brazil., Gelfuso GM; Laboratório de Medicamentos, Alimentos e Cosméticos, Universidade de Brasília, Brasília 70910-900, DF, Brazil., Saldanha-Araujo F; Laboratório de Hematologia e Células-Tronco, Faculdade de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, DF, Brazil.
المصدر: Biomedicines [Biomedicines] 2024 May 04; Vol. 12 (5). Date of Electronic Publication: 2024 May 04.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI AG Country of Publication: Switzerland NLM ID: 101691304 Publication Model: Electronic Cited Medium: Print ISSN: 2227-9059 (Print) Linking ISSN: 22279059 NLM ISO Abbreviation: Biomedicines Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI AG, [2013]-
مستخلص: Ibrutinib, a tyrosine kinase inhibitor with a broad spectrum of action, has been successfully explored to treat hematological and solid cancers. Herein, we investigated the anti-cancer effect of Ibrutinib on melanoma cell lines. Cytotoxicity was evaluated using the MTT assay. Apoptosis, mitochondrial membrane potential, reactive oxygen species (ROS) production, cell proliferation, and cell cycle stages were determined by flow cytometry. LDH release and Caspase 3/7 activity were determined by colorimetric and luminescent assays, respectively. Cell migration was evaluated by wound scratch assay. Gene expression was determined by real-time PCR. Gene Ontology (GO) enrichment analysis of melanoma clinical samples was performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID). MTT assays showed that Ibrutinib is toxic for MeWo, SK-MEL-28, and WM164 cells. The annexin V/PI staining, Caspase 3/7 activity, and LDH release in MeWo cells revealed that apoptosis is the primary mechanism of death caused by Ibrutinib. Corroborating such observation, we identified that Ibrutinib treatment impairs the mitochondrial membrane potential of such cells and significantly increases the transcriptional levels of the pro-apoptotic factors ATM , HRK , BAX , BAK , CASP3 , and CASP8 . Furthermore, Ibrutinib showed antimetastatic potential by inhibiting the migration of MeWo cells. Finally, we performed a functional enrichment analysis and identified that the differential expression of Ibrutinib-target molecules is associated with enrichment of apoptosis and necrosis pathways in melanoma samples. Taken together, our results clearly suggest that Ibrutinib can be successfully explored as an effective therapeutic approach for melanomas.
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معلومات مُعتمدة: 00193-00000721/2021-04 Fundação de Amparo à Pesquisa do Distrito Federal; 302317/2022-8 Conselho Nacional de Desenvolvimento Científico e Tecnológico
فهرسة مساهمة: Keywords: BTK; Ibrutinib; MeWo; melanoma; skin cancer
تواريخ الأحداث: Date Created: 20240525 Latest Revision: 20240527
رمز التحديث: 20240527
مُعرف محوري في PubMed: PMC11117653
DOI: 10.3390/biomedicines12051012
PMID: 38790974
قاعدة البيانات: MEDLINE
الوصف
تدمد:2227-9059
DOI:10.3390/biomedicines12051012