CRISPR-Cas9-mediated ALMS1 knockout inhibits TGF-β signalling and epithelial-mesenchyme transition.

ABSTRACT: In this project we evaluated the proteomic profiling with TGF-β stimuli at 24h in a CRISPR-Cas9 model for ALMS1 gene in HeLa cells. Proteomic results showed a majority inhibition of downstream regulated pathways by the TGF-β, associating the protein coding genes (PCG) with processes like focal adhesion or cell-substrate adherens junction. Finally, EMT biomarkers like VIM, DSP, EDIL3 and SNAI1 had the opposite pattern to what would be expected when activating the EMT. In conclusion, seems that the depletion of ALMS1 could be inhibiting the signals transduction through the TGF -β and the routes regulated downstream by it such as the EMT.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Cervical Adenocarcinoma

SUBMITTER: Brais Bea Mascato  

LAB HEAD: Diana Valverde Pérez

PROVIDER: PXD024964 | Pride | 2023-03-11

REPOSITORIES: Pride