Laboratório de Sinalização e Plasticidade Celular

O Laboratório de Sinalização e Plasticidade Celular da UFRGS está localizado dentro do Departamento de Biofísica do Instituto de Biociências da UFRGS e afiliado ao Centro de Biotecnologia da UFRGS e tem por objetivo o estudo das vias de sinalização celular com especial foco em câncer e reprogramação celular.

Laboratório de Sinalização e Plasticidade Celular - Sala 107 - Prédio 43431 - Departamento de Biofísica, Instituto de Biociências
Universidade Federal do Rio Grande do Sul, UFRGS.
Av. Bento Gonçalves, 9500, 91501-970, Porto Alegre, Rio Grande do Sul, Brasil

Telefone: ++55 51 3308 7620 (Laboratório)
++55 51 3308 7613 (Sala Dr. Guido Lenz)


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Single-cell analysis challenges the connection between autophagy and senescence induced by DNA damage.

Abstract: Autophagy and senescence have been described as central features of cell biology, but the interplay between these mechanisms remains obscure. Using a therapeutically relevant model of DNA damage-induced senescence in human glioma cells, we demonstrated that acute treatment with temozolomide induces DNA damage, a transitory activation of PRKAA/AMPK-ULK1 and MAPK14/p38 and the sustained inhibition of AKT-MTOR. This produced a transient induction of autophagy, which was followed by senescence. However, at the single cell level, this coordinated transition was not observed, and autophagy and senescence were triggered in a very heterogeneous manner. Indeed, at a population level, autophagy was highly negatively correlated with senescence markers, while in single cells this correlation did not exist. The inhibition of autophagy triggered apoptosis and decreased senescence, while its activation increased temozolomide-induced senescence, showing that DNA damage-induced autophagy acts by suppressing apoptosis

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Cell Death & Differentiation Review - Autophagy and genomic integrity
A T Vessoni, E C Filippi-Chiela, C FM Menck and G Lenz:

Abstract: DNA lesions, constantly produced by endogenous and exogenous sources, activate the DNA damage response (DDR), which involves detection, signaling and repair of the damage. Autophagy, a lysosome-dependent degradation pathway that is activated by stressful situations such as starvation and oxidative stress, regulates cell fate after DNA damage and also has a pivotal role in the maintenance of nuclear and mitochondrial genomic integrity. Here, we review important evidence regarding the role played by autophagy in preventing genomic instability and tumorigenesis, as well as in micronuclei degradation. Several pathways governing autophagy activation after DNA injury and the influence of autophagy upon the processing of genomic lesions are also discussed herein. In this line, the mechanisms by which several proteins participate in both DDR and autophagy, and the importance of this crosstalk in cancer and neurodegeneration will be presented in an integrated fashion. At last, we present a hypothetical model of the role played by autophagy in dictating cell fate after genotoxic stress.

Journals News
Cancer Cell
Nature Reviews Cancer