Cáncer y mitocondria: un aspecto central para el desarrollo y crecimiento tumoral

Sofía Isabel Freyre-Bernal, Jhan Sebastián Saavedra-Torres, Luisa Fernanda Zúñiga-Cerón, Andrés Felipe Olaya-Castañeda, Carolina Salguero

Resumen


Se sabe que las células tumorales consumen más glucosa que las no tumorales. Además, las células tumorales expresan isoformas embrionarias de enzimas para la glucólisis, permitiendo su mayor actividad y obtención de energía en los diversos procesos cancerígenos. Algunos autores han sugerido que la hipoxia del tumor actúa como regulador del metabolismo energético y que puede redirigir a las células tumorales a utilizar la glucólisis como fuente de provisión de ATP cuando hay limitación de oxígeno. Otros autores sugieren que ese es el resultado de mutaciones en oncogenes, genes supresores y enzimas de la vía glucolítica o del metabolismo oxidativo mitocondrial (Myc, Akt, p53, HIF1-α). La aplicación de la tomografía de emisión de positrones (PET) en los servicios de medicina nuclear y radiología ha permitido usar la mitocondria como un organelo para el diagnóstico de cáncer cuantificando una mayor captación de glucosa por las células tumorales respecto del tejido no tumoral adyacente, mediante el uso del análogo radioactivo no metabolizable de la glucosa (18FDG, 18F-2-desoxiglucosa). Así pues, las investigaciones se han centrado en el metabolismo alterado como parte del desarrollo y crecimiento tumoral con el objetivo de inhibir la progresión a la metástasis de esta patología en los pacientes que no se pueden recuperar recibiendo tratamiento con quimioterapia y la radioterapia. El objetivo de esta revisión documental consiste en resaltar las generalidades e importancia de las mitocondrias en los mecanismos que promueven el cáncer.

 

Cancer and mitochondria: a central aspect to tumor development and growth


Abstract

Tumor cells consume more glucose than the non-tumor cells. In addition, tumor cells express isoforms of embryonic glycolytic enzymes with higher activity to obtain energy in the various carcinogenic processes. Some authors have suggested that hypoxia of the tumor acts as a regulator of energy metabolism and can redirect to tumor cells to use the glycolysis as source for the supply of ATP when there is limitation of oxygen. In contrast, other authors suggest that this phenomena is the result of mutations in oncogenes, tumor suppressor genes and enzymes of the glycolytic pathway or oxidative metabolism mitochondrial including Myc, Akt, p53, HIF1-α. The application of Positron Emission Tomography (PET) in nuclear medicine services and radiology has allowed the use of mitochondria as an organelle that serves to diagnose cancer, quantify greater uptake of glucose by tumor cells on adjacent non-tumor tissue using analogue radioactive non-metabolizable glucose (18FDG, 18F-2-desoxiglucosa). Such research has focused on altered metabolism as part of development and tumor growth to inhibit the progression of cancer to metastases in patients that cannot be recovered by chemotherapy and radiation therapy. The aim of this review is to highlight the generalities and importance of mitochondria in the mechanisms that promote cancer.


Palabras clave


mitocondria, adenosín trifosfato, biogénesis de organelos, apoptosis, cáncer, medicina nuclear, mitochondria, adenosine triphosphate, organelle biogenesis, apoptosis, cancer, nuclear medicine

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Referencias


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