Publications by authors named "G Del Sal"
Article Synopsis
- Micronuclei (MN) are formed through various mechanisms, and their frequent presence in tumors suggests they might actively contribute to cancer progression rather than being just passive byproducts.
- This study highlights how damages during cell division can lead to the accumulation of Emerin in MN, which lack Lamin A/C and feature the Lamin-B receptor and Sec61β.
- Emerin mislocalization to MN is linked to a poor prognosis in prostate cancer patients and is associated with increased migratory and invasive behaviors of tumor cells, particularly in environments rich in collagen.
Conventional type 1 dendritic cells (cDC1) are critical regulators of anti-tumoral T-cell responses. The structure and abundance of intercellular contacts between cDC1 and CD8 T cells in cancer tissues is important to determine the outcome of the T-cell response. However, the molecular determinants controlling the stability of cDC1-CD8 interactions during cancer progression remain poorly investigated.
View Article and Find Full Text PDFThe P53-destabilizing TBC1D15-NOTCH protein interaction promotes self-renewal of tumor-initiating stem-like cells (TICs); however, the mechanisms governing the regulation of this pathway have not been fully elucidated. Here, we show that TBC1D15 stabilizes NOTCH and c-JUN through blockade of E3 ligase and CDK8 recruitment to phosphodegron sequences. Chromatin immunoprecipitation (ChIP-seq) analysis was performed to determine whether TBC1D15-dependent NOTCH1 binding occurs in TICs or non-TICs.
View Article and Find Full Text PDFBackground: New drugs to tackle the next pathway or mutation fueling cancer are constantly proposed, but 97% of them are doomed to fail in clinical trials, largely because they are identified by cellular or in silico screens that cannot predict their in vivo effect.
Methods: We screened an Adeno-Associated Vector secretome library (> 1000 clones) directly in vivo in a mouse model of cancer and validated the therapeutic effect of the first hit, EMID2, in both orthotopic and genetic models of lung and pancreatic cancer.
Results: EMID2 overexpression inhibited both tumor growth and metastatic dissemination, consistent with prolonged survival of patients with high levels of EMID2 expression in the most aggressive human cancers.