Article
Mitochondrial genome instability in colorectal adenoma and adenocarcinoma
Registro en:
ARAUJO, L. F. et al. Mitochondrial genome instability in colorectal adenoma and adenocarcinoma. Tumor Biology, v. 36, n. 11, p. 8869-8879, 2015.
1010-4283
10.1007/s13277-015-3640-7
Autor
Araujo, Luiza Ferreira de
Fonseca, Aline Simonete
Muys, Bruna Rodrigues
Plaça, Jessica Rodrigues
Bueno, Rafaela de Barros e Lima
Lorenzi, Julio Cesar Cetrulo
Santos, Anemari Ramos Dinarte dos
Molfetta, Greice Andreotti de
Zanette, Dalila Lucíola
Souza, Jorge Estefano Santana de
Valente, Valeria
Silva Junior, Wilson Araujo da
Resumen
Zanette, Dalila Lucíola “Documento produzido em parceria ou por autor vinculado à Fiocruz, mas não consta à informação no documento”. The National Council for Scientific and Technological Development (CNPq), grant #573754/2008-0; by
grants #2008/57877-3 and #2013/08135-2, São Paulo Research Foundation (FAPESP); and by Research Support of the University Sao Paulo, CISBi-NAP/USP #12.1.25441.01.2. Mitochondrial dysfunction is regarded as a hallmark of cancer progression. In the current study, we evaluated mitochondrial genome instability and copy number in colorectal cancer using Next Generation Sequencing approach and qPCR, respectively. The results revealed higher levels of heteroplasmy and depletion of the relative mtDNA copy number in colorectal adenocarcinoma. Adenocarcinoma samples also presented an increased number of mutations in nuclear genes encoding proteins which functions are related with mitochondria fusion, fission and localization. Moreover, we found a set of mitochondrial and nuclear genes, which cooperate in the same mitochondrial function simultaneously mutated in adenocarcinoma. In summary, these results support an important role for mitochondrial function and genomic instability in colorectal tumorigenesis.