Anita Vega-Miranda
Research Subjects
Research Interests
Anita Vega-Miranda has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Criselda Mendoza-Milla
Research Unit, Signal Transduction Laboratory, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Calzada de Tlalpan 4502, Belisario Domínguez Sección XVI, Tlalpan, Mexico City 14080, Mexico
1 shared publication - Irlanda Peralta-Arrieta
Laboratorio de Transducción de Señales, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico
1 shared publication - Rebeca López-Marure
Departamento de Fisiología, Instituto Nacional de Cardiología Ignacio Chávez, Ciudad de México, Mexico
1 shared publication - Zaira Colín-Val
Centro Universitario del Sur, Universidad de Guadalajara
1 shared publication
Latest Publications
- Open Access
- 26 September 2023
- Published by MDPI AG in Preprints.org
Dehydroepiandrosterone Suppresses Proliferation and Migration while Promoting Autophagy in Lung Cancer Cells
Lung cancer is a prevalent and aggressive neoplasm worldwide, contributing to significant mortality rates. Dehydroepiandrosterone (DHEA) constitutes the bulk of the steroid hormone in human plasma, has a robust antiproliferative effect, and induces cell death in various tumor cells. However, its role in lung cancer cells remains unexplored. This study aimed to investigate the influence of DHEA on the proliferation, viability, autophagy, and migration of several lung cancer cell lines, including A549, HCC827, and NCI-H2347. Cell proliferation was assessed through crystal violet staining; cell number and viability were evaluated using trypan blue staining; viability was confirmed by MTT reduction, a method that is also an indicator of metabolic activity; migration was assessed via a wound healing assay. Autophagy was evaluated using a specific kit, while cell death was determined by annexin-V-FITC/propidium iodide staining and caspase-3/7 activity assay. The results indicate that DHEA significantly reduced proliferation, cell number, metabolic activity, and migration in all examined lung tumor cells. These effects correlate with an increased autophagy induced by DHEA. No signs of apoptosis or necrosis were observed across the range of DHEA concentrations used. Although these findings are preliminary, they suggest that DHEA could hold promise as an alternative treatment option for various subtypes of lung cancer.
- 26 September 2023
- Published by MDPI AG in Preprints.org
Open AccessDehydroepiandrosterone Suppresses Proliferation and Migration while Promoting Autophagy in Lung Cancer Cells
Lung cancer is a prevalent and aggressive neoplasm worldwide, contributing to significant mortality rates. Dehydroepiandrosterone (DHEA) constitutes the bulk of the steroid hormone in human plasma, has a robust antiproliferative effect, and induces cell death in various tumor cells. However, its role in lung cancer cells remains unexplored. This study aimed to investigate the influence of DHEA on the proliferation, viability, autophagy, and migration of several lung cancer cell lines, including A549, HCC827, and NCI-H2347. Cell proliferation was assessed through crystal violet staining; cell number and viability were evaluated using trypan blue staining; viability was confirmed by MTT reduction, a method that is also an indicator of metabolic activity; migration was assessed via a wound healing assay. Autophagy was evaluated using a specific kit, while cell death was determined by annexin-V-FITC/propidium iodide staining and caspase-3/7 activity assay. The results indicate that DHEA significantly reduced proliferation, cell number, metabolic activity, and migration in all examined lung tumor cells. These effects correlate with an increased autophagy induced by DHEA. No signs of apoptosis or necrosis were observed across the range of DHEA concentrations used. Although these findings are preliminary, they suggest that DHEA could hold promise as an alternative treatment option for various subtypes of lung cancer.