12 results on '"Carrera, Ana Clara"'
Search Results
2. Towards the Search for Potential Biomarkers in Osteosarcoma: State-of-the-Art and Translational Expectations
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Pekarek, Leonel, primary, De la Torre-Escuredo, Basilio, additional, Fraile-Martinez, Oscar, additional, García-Montero, Cielo, additional, Saez, Miguel A., additional, Cobo-Prieto, David, additional, Guijarro, Luis G., additional, Saz, Jose V., additional, De Castro-Martinez, Patricia, additional, Torres-Carranza, Diego, additional, Pekarek, Tatiana, additional, Carrera, Ana Clara, additional, Alvarez-Mon, Melchor, additional, and Ortega, Miguel A., additional
- Published
- 2022
- Full Text
- View/download PDF
3. Role of NRF2 in Lung Cancer
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Sánchez-Ortega, Miriam, primary, Carrera, Ana Clara, additional, and Garrido, Antonio, additional
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- 2021
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4. A promoter DNA demethylation landscape of human hematopoietic differentiation
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Calvanese, Vincenzo, Fernández, Agustín F., Urdinguio, Rocío G., Suárez-Alvarez, Beatriz, Mangas, Cristina, Pérez-García, Vicente, Bueno, Clara, Montes, Rosa, Ramos-Mejía, Verónica, Martínez-Camblor, Pablo, Ferrero, Cecilia, Assenov, Yassen, Bock, Christoph, Menendez, Pablo, Carrera, Ana Clara, Lopez-Larrea, Carlos, and Fraga, Mario F.
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- 2012
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5. Targeted depletion of PIK3R2 induces regression of lung squamous cell carcinoma
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Vallejo-Díaz, Jesús, primary, Olazabal-Morán, Manuel, additional, Cariaga-Martínez, Ariel E., additional, Pajares, María J., additional, Flores, Juana M., additional, Pio, Ruben, additional, Montuenga, Luis M., additional, and Carrera, Ana Clara, additional
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- 2016
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6. Generación de vectores para la identificación de interacciones diferenciales de las isoformas de p85
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Vallejo Díaz, Jesús and Carrera, Ana Clara
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Switch ,Pull down ,Pharmacy ,p85β ,pEBG(GST) ,Farmacia ,PI3K ,Biology ,Biología y Biomedicina ,Tinción argéntica - Abstract
PIK3R2 codifica la subunidad reguladora p85β de PI3K, un enzima que genera 3-polifosfoinosítidos en la membrana plasmática. La activación de PI3K dispara los mecanismos de supervivencia celular y migración. La sobreexpresión de p85β se ha observado en diferentes tipos de cáncer como mama y colon, y esta expresión elevada de p85β se correlaciona con un aumento de la señalización de PI3K y la progresión tumoral. La subunidad p85α se expresa de forma mayoritaria en las células normales, pero recientemente se ha demostrado que en algunos tumores se reducen los niveles de expresión de p85α y aumenta el de p85β (“p85β switch”). Este cambio en la expresión de p85 está correlacionado con la invasión y la progresión tumoral. En este trabajo trataremos de obtener herramientas de biología molecular que nos permitan determinar las interacciones diferenciales entre p85α y p85β con el objetivo de determinar la implicación de p85β en la supervivencia, migración e invasión celular
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- 2013
7. A promoter DNA demethylation landscape of human hematopoietic differentiation
- Author
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Calvanese, Vincenzo, primary, Fernández, Agustín F., additional, Urdinguio, Rocío G., additional, Suárez-Alvarez, Beatriz, additional, Mangas, Cristina, additional, Pérez-García, Vicente, additional, Bueno, Clara, additional, Montes, Rosa, additional, Ramos-Mejía, Verónica, additional, Martínez-Camblor, Pablo, additional, Ferrero, Cecilia, additional, Assenov, Yassen, additional, Bock, Christoph, additional, Menendez, Pablo, additional, Carrera, Ana Clara, additional, Lopez-Larrea, Carlos, additional, and Fraga, Mario F., additional
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- 2011
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8. Phosphoinositide 3‐kinase gamma; participates in T cell receptor‐induced T cell activation.
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Alcazar, Isabela, primary, Marqués, Miriam, additional, Kumar, Amit, additional, Hirsch, Emilio, additional, Wymann, Matthias, additional, Carrera, Ana Clara, additional, and Barber, Domingo Francisco, additional
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- 2008
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9. Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities.
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Chen, Yongfeng, Li, Jing, Zhao, Zhiqiang, Kalyuzhny, Alexander E., Carrera, Ana Clara, and Garrido, Antonio
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LYMPHOBLASTIC leukemia ,ACUTE leukemia ,HEMATOPOIETIC stem cells ,DRUG side effects ,OXIDATION-reduction reaction - Abstract
Acute lymphoblastic leukemia (ALL) is a hematological malignancy originating from B- or T-lymphoid progenitor cells. Recent studies have shown that redox dysregulation caused by overproduction of reactive oxygen species (ROS) has an important role in the development and progression of leukemia. The application of pro-oxidant therapy, which targets redox dysregulation, has achieved satisfactory results in alleviating the conditions of and improving the survival rate for patients with ALL. However, drug resistance and side effects are two major challenges that must be addressed in pro-oxidant therapy. Oxidative stress can activate a variety of antioxidant mechanisms to help leukemia cells escape the damage caused by pro-oxidant drugs and develop drug resistance. Hematopoietic stem cells (HSCs) are extremely sensitive to oxidative stress due to their low levels of differentiation, and the use of pro-oxidant drugs inevitably causes damage to HSCs and may even cause severe bone marrow suppression. In this article, we reviewed research progress regarding the generation and regulation of ROS in normal HSCs and ALL cells as well as the impact of ROS on the biological behavior and fate of cells. An in-depth understanding of the regulatory mechanisms of redox homeostasis in normal and malignant HSCs is conducive to the formulation of rational targeted treatment plans to effectively reduce oxidative damage to normal HSCs while eradicating ALL cells. [ABSTRACT FROM AUTHOR]
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- 2021
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10. KLF4 Regulates Metabolic Homeostasis in Response to Stress.
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Blum, Andrew, Mostow, Kate, Jackett, Kailey, Kelty, Estelle, Dakpa, Tenzing, Ryan, Carly, Hagos, Engda, Carrera, Ana Clara, and Khalimonchuk, Oleh
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GLUCOSE transporters ,REACTIVE oxygen species ,HOMEOSTASIS ,TRANSCRIPTION factors ,WESTERN immunoblotting ,GLYCOLYSIS ,ONCOGENES - Abstract
Cancerous cells are detrimental to the human body and can be incredibly resilient against treatments because of the complexities of molecular carcinogenic pathways. In particular, cancer cells are able to sustain increased growth under metabolic stress due to phenomena like the Warburg effect. Krüppel-like factor 4 (KLF4), a context-dependent transcription factor that can act as both a tumor suppressor and an oncogene, is involved in many molecular pathways that respond to low glucose and increased reactive oxygen species (ROS), raising the question of its role in metabolic stress as a result of increased proliferation of tumor cells. In this study, metabolic assays were performed, showing enhanced efficiency of energy production in cells expressing KLF4. Western blotting showed that KLF4 increases the expression of essential glycolytic proteins. Furthermore, we used immunostaining to show that KLF4 increases the localization of glucose transporter 1 (GLUT1) to the cellular membrane. 2′,7′-Dichlorodihydrofluorescein diacetate (H
2 DCF-DA) was used to analyze the production of ROS, and we found that KLF4 reduces stress-induced ROS within cells. Finally, we demonstrated increased autophagic death in KLF4-expressing cells in response to glucose starvation. Collectively, these results relate KLF4 to non-Warburg metabolic behaviors that support its role as a tumor suppressor and could make KLF4 a target for new cancer treatments. [ABSTRACT FROM AUTHOR]- Published
- 2021
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11. Role of Reductive versus Oxidative Stress in Tumor Progression and Anticancer Drug Resistance.
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Chun, Kyung-Soo, Kim, Do-Hee, Surh, Young-Joon, Carrera, Ana Clara, and Garrido, Antonio
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OXIDATIVE stress ,CANCER invasiveness ,DRUG resistance ,ANTINEOPLASTIC agents ,CANCER cell proliferation - Abstract
Redox homeostasis is not only essential for the maintenance of normal physiological functions, but also plays an important role in the growth, survival, and therapy resistance of cancer cells. Altered redox balance and consequent disruption of redox signaling are implicated in the proliferation and progression of cancer cells and their resistance to chemo- and radiotherapy. The nuclear factor erythroid 2 p45-related factor (Nrf2) is the principal stress-responsive transcription factor that plays a pivotal role in maintaining cellular redox homeostasis. Aberrant Nrf2 overactivation has been observed in many cancerous and transformed cells. Uncontrolled amplification of Nrf2-mediated antioxidant signaling results in reductive stress. Some metabolic pathways altered due to reductive stress have been identified as major contributors to tumorigenesis. This review highlights the multifaceted role of reductive stress in cancer development and progression. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
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12. Papel de la proteína p85β en el cáncer de células escamosas de pulmón
- Author
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Vallejo Díaz, Jesús, Carrera, Ana Clara (dir.), UAM. Departamento de Biología Molecular, and Carrera, Ana Clara
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Células cancerosas - Tesis doctorales ,Inhibidores - Tesis doctorales ,Cáncer de pulmón - Tesis doctorales ,Biología y Biomedicina / Biología - Abstract
Tesis doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de lectura: 09-03-2018, El cáncer de pulmón es el tipo de cáncer que, anualmente, registra una mayor tasa de mortalidad en el mundo. Este tipo de cáncer se clasifica, en base a su histología, en cáncer de células pequeñas y no pequeñas, y, dentro de este último grupo, en adenocarcinoma, carcinoma de células grandes y carcinoma de células escamosas (SqCLC). Las enzimas fosfatidilinositol-3-quinasa (PI3K) son una familia de proteínas con actividad quinasa que están implicadas en múltiples funciones celulares como proliferación, migración, supervivencia, tráfico vesicular y biosíntesis de proteínas. Las PI3K de clase IA se componen de una subunidad catalítica (p110) y una subunidad reguladora (p85), ambas con varias isoformas. En el caso de p85, tanto p85α como p85β se expresan de manera ubicua, aunque el nivel de expresión de la isoforma alfa es mayor que la de beta en condiciones basales. Sin embargo, en el cáncer de mama y de colon se ha descrito un cambio en los niveles de expresión de ambas isoformas, siendo p85β la expresada mayoritariamente. En esta tesis se muestra que en el SqCLC también hay un cambio de expresión de p85α y p85β. En los estudios in vitro, el silenciamiento de p85β provocó una reducción en los niveles de activación de la ruta de PI3K en varias líneas de SqCLC. En los estudios in vivo, se determinó que p85β, y no p85α, está implicada en el mantenimiento de la masa tumoral, observando una regresión en la mayoría de las líneas de SqCLC tras el silenciamiento de p85β. Por su parte, el silenciamiento de p85α no tuvo efecto, apoyando la hipótesis de que la subunidad p85β es la implicada en la progresión tumoral en el SqCLC. Existen inhibidores de la ruta de PI3K, en diferentes etapas de ensayos clínicos (alguno aprobado para su uso), dirigidos contra las diferentes isoformas de p110, o contra otros efectores de la ruta, como Akt o mTOR. Uno de los principales problemas de estos inhibidores es que generan resistencias y reactivación de la ruta, por lo que proponemos el desarrollo de agentes interferentes contra la subunidad p85β. A diferencia del tratamiento con inhibidores, la interferencia de p85β no produjo reactivación de la ruta de PI3K a tiempos largos. Además, en estudios in vivo, se observó que el silenciamiento de p85β producía regresión tumoral y, a largo plazo, tampoco reactivaba ruta de PI3K. Nuestros datos sugieren que la subunidad reguladora p85β es una nueva diana terapéutica para el tratamiento de SqCLC, Lung cancer exhibits the highest mortality index worldwide among different types. Based on histological analysis, lung cancer is classified as small-cell and non-small-cell lung cancers; this second group is comprised by lung adenocarcinoma, large-cell lung carcinoma and squamous cell lung carcinoma (SqCLC). The PI3K (phosphatidylinositol 3-kinase) enzymes are a protein family with kinase activity that are involved in several cell functions such as proliferation, migration, survival, vesicle trafficking and protein biosynthesis. PI3K class IA is composed of a catalytic subunit (p110) and a regulatory subunit (p85), and both have various isoforms. In the case of p85, both p85α and p85β are expressed in all cells, although in normal cells p85α expression is higher than that of p85β. In breast and colon carcinoma, however, there is a switch in isoform expression, with p85β the most highly expressed. In this thesis, we show that there is also a p85α/p85β isoform switch in SqCLC. Our in vitro studies show that p85β depletion reduces the activation state of the PI3K pathway in some SqCLC cell lines. In in vivo studies, we determined that p85β, and not p85α, is involved in the maintenance of tumour survival, with tumour regression in most xenografts derived from SqCLC cell lines after p85β depletion. p85α depletion had no effect, which supports our hypothesis that the p85β subunit is the isoform implicated in SqCLC tumour progression. Numerous PI3K pathway inhibitors are currently being tested in different clinical trial phases (some have already been approved for clinical use); these inhibitors target different p110 isoforms or other PI3K pathway effectors, such as Akt or mTOR. One of the most important problems of inhibitors is that they produce resistance and PI3K pathway reactivation; for this reason, we propose to develop agents that interfere with the p85β regulatory subunit. In contrast to inhibitors, interference with p85β did not produce PI3K pathway reactivation after long treatment periods. In addition, in in vivo assays, p85β depletion produced tumour shrinkage and, after long treatment periods, PI3K pathway activity continued to be repressed. These findings suggest the p85β regulatory subunit as a therapeutic target for treatment of squamous cell lung carcinoma
- Published
- 2018
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