Pauperization of Emerin from nuclear envelope drives prostate cancer cell migration and invasiveness
Nastaly, P.; Popeda, M.; Kowalski, K.; Wenta, T.; Beznoussenko, G.; Rychlowski, M.; Mironov, A.; Lavagnino, Z.; Barozzi, S.; Richert, J.; Bertolio, R.; Szade, J.; Miszewski, K.; Matuszewski, M.; Zaczek, A. J.; Braga, L.; Del Sal, G.; Bednarz-Knoll, N.; Maiuri, P.
Show abstract
Micronuclei (MN) can arise from many causes, including the breakage of aberrant cytokinetic chromatin bridge. The frequent observation of MN in tumors raises the specter that they might not merely be passive elements but could instead play active roles in tumor progression. Here, we test the hypothesis that the presence of micronuclei could induce specific phenotypic and functional changes to the cell and lead to increased cancer invasive potential. With a variety of imaging and molecular methods in vitro and in clinical samples from prostate cancer (PCa) patients, we show that chromosome bridge resolution can lead to EMD accumulation and formation of EMD-rich MN. Such structure is negative for Lamin A/C and positive for LBR and Sec6{beta}. It can cause EMD pauperization from NE affecting migratory and invasive properties of a cell and can be translated to PCa patients poor prognosis.
Matching journals
The top 9 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- A single-cell atlas of the mouse and human prostate reveals heterogeneity and conservation of epithelial progenitors 96%
- Defining cellular population dynamics at single cell resolution during prostate cancer progression 95%
- The CIC-ERF co-deletion underlies fusion independent activation of ETS family member, ETV1, to drive prostate cancer progression 95%
Similar papers in this journal
Similar papers in this journal
- Single-cell ATAC and RNA sequencing reveal pre-existing and persistent subpopulations of cells associated with relapse of prostate cancer 96%
- Transcriptional network involving ERG and AR orchestrates Distal-Less Homeobox 1 mediated prostate cancer progression. 96%
- Role of Specialized mSWI/SNF Complexes in Prostate Cancer Lineage Plasticity 95%
Similar papers in this journal
- BAZ2A association with H3K14ac is required for the transition of prostate cancer cells into a cancer stem-like state 96%
- Rarγ-Foxa1 signaling promotes luminal identity in prostate progenitors and is disrupted in prostate cancer 95%
- The histone methyltransferase DOT1L regulates chromatin reorganization and gene expression during the postmeiotic differentiation of male germ cells 93%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.