Termocronologia por traços de fissão em apatitas na região do Arco de Ponta Grossa, entre os alinhamentos de Guapiara e São Jerônimo-Curiúva

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Evolução da tectônica rúptil no nordeste do Brasil baseada na termocronologia por traço de fissão em apatita

Results of apatite fission tracks from twelve samples collected across a Borborema Province transect, northeastern Brazil, revealed two major paleothermal events: a cooling event occurred between Albian and late Cenomanian (110 - 80 Ma) and a second cooling event starting on early Paleocene (66 Ma). Given the wide expression of the studied area (sampling trend along four brazilian states) a correlation between the distribution of fission track data and the current geological / geomorphological scenario was made possible, considering the area’s tectono - stratigraphic past and its thermochronologic evolution until now. The fact that the employed thermochronologic tool relates to a relatively shallow geothermometer, substancially information for understanding the behavior of basement brittle tectonic was achieved. These data were used to analyze faults origin and reactivation, associated with sedimentary basins evolution in the context of South America - Africa continental breakup.

Loss of Expression and Function of SOCS3 Is an Early Event in HNSCC: Altered Subcellular Localization as a Possible Mechanism Involved in Proliferation, Migration and Invasion

Background: Suppressor of cytokine signaling 3 (SOCS3) is an inducible endogenous negative regulator of signal transduction and activator of transcription 3 (STAT3). Epigenetic silencing of SOCS3 has been shown in head and neck squamous cell carcinoma (HNSCC), which is associated with increased activation of STAT3. There is scarce information on the functional role of the reduction of SOCS3 expression and no information on altered subcellular localization of SOCS3 in HNSCC.Methodology/Principal Findings: We assessed endogenous SOCS3 expression in different HNSCC cell lines by RT-qPCR and western blot. Immunofluorescence and western blot were used to study the subcellular localization of endogenous SOCS3 induced by IL-6. Overexpression of SOCS3 by CMV-driven plasmids and siRNA-mediated inhibition of endogenous SOCS3 were used to verify the role of SOCS3 on tumor cell proliferation, viability, invasion and migration in vitro. In vivo relevance of SOCS3 expression in HNSCC was studied by quantitative immunohistochemistry of commercially-available tissue microarrays. Endogenous expression of SOCS3 was heterogeneous in four HNSCC cell lines and surprisingly preserved in most of these cell lines. Subcellular localization of endogenous SOCS3 in the HNSCC cell lines was predominantly nuclear as opposed to cytoplasmic in non-neoplasic epithelial cells. Overexpression of SOCS3 produced a relative increase of the protein in the cytoplasmic compartment and significantly inhibited proliferation, migration and invasion, whereas inhibition of endogenous nuclear SOCS3 did not affect these events. Analysis of tissue microarrays indicated that loss of SOCS3 is an early event in HNSCC and was correlated with tumor size and histological grade of dysplasia, but a considerable proportion of cases presented detectable expression of SOCS3.Conclusion: Our data support a role for SOCS3 as a tumor suppressor gene in HNSCC with relevance on proliferation and invasion processes and suggests that abnormal subcellular localization impairs SOCS3 function in HNSCC cells.