Search bioRxiv⌕ Search

Biology subjects

Giacomelli, C.

Publications and source records attributed to Giacomelli, C..

2 recordsLinked to original sources

Global quantification of mammalian gene expression noise

Even cells of the same type growing in the same environment show cell-to-cell differences in protein abundance, a phenomenon known as gene expression noise. This variability can be decomposed into intrinsic components, reflecting molecular randomness, and extrinsic components, arising from differences in cellular state. While gene expression noise has been studied genome-wide in microbes, its global organization remains largely unknown in mammalian cells. Here, we develop a spike-in-based stable isotope single-cell proteomics approach that enables robust quantification of protein-level gene expression noise across thousands of human proteins. We find that protein noise scales inversely with abundance until reaching a plateau, consistent with an extrinsic noise floor and conserved scaling principles observed in bacteria and yeast. Cell cycle stage and cell size contribute substantially to protein variability but do not fully account for the observed heterogeneity. Gene-specific features such as mRNA and protein half-lives and translation efficiency show only weak associations with protein noise, and variability at the mRNA level is a weak predictor of protein variability. Instead, protein noise is largely extrinsic, with coordinated variation across proteins encoding biologically organized cellular states. Consistently, coordinated proteome programs predict intercellular differences in proteome dynamics, linking protein variability to cellular function. Together, these results provide a proteome-wide view of gene expression noise in mammalian cells, establishing that protein-level variability encodes structured and functionally relevant differences in cellular state.

systems biology↗

Coordinated regulation of WNT/β-catenin, c-Met, and Integrin signalling pathways by miR-193b controls triple negative breast cancer metastatic traits

BackgroundTriple Negative Breast Cancer (TNBC) is the most aggressive subtype of Breast Cancer (BC). Treatment options for TNBC patients are limited and further insights into disease aetiology are needed to develop better therapeutic approaches. microRNAs ability to regulate multiple targets could hold a promising discovery approach to pathways relevant for TNBC aggressiveness. Thus, we address the role of miRNAs in controlling signalling pathways and phenotypes relevant to the biology of TNBC. MethodsTo identify miRNAs regulating WNT/{beta}-catenin, c-Met, and integrin signalling pathways, we performed a high-throughput targeted proteomic approach, investigating the effect of 800 miRNAs on the expression of 62 proteins in the MDA-MB-231 TNBC cell line. We then developed a novel network analysis, Pathway Coregulatory (PC) score, to detect miRNAs regulating the three pathways. Using in vitro assays for cell growth, migration, apoptosis, and stem-cell content, we validated the function of candidate miRNAs. Bioinformatic analyses using BC patients datasets were employed to assess expression of miRNAs as well as their pathological relevance in TNBC patients. ResultsWe identified six candidate miRNAs coordinately regulating the three signalling pathways. Quantifying cell growth of three TNBC cell lines upon miRNA gain-of-function experiments, we characterised miR-193b as a strong and consistent repressor of this phenotype. Importantly, the effects of miR-193b were stronger than chemical inhibition of the individual pathways. We further demonstrated that miR-193b induced apoptosis, repressed migration, and regulated stem-cell markers in MDA-MB-231 cells. Furthermore, miR-193b expression was the lowest in patients classified as TNBC or Basal compared to other subtypes when classified by PAM50 signatures. Gene Set Enrichment Analysis showed that miR-193b expression was significantly associated with reduced activity of of WNT/{beta}-catenin and c-Met signalling pathways in TNBC patients. ConclusionsIntegrating miRNA-mediated effects and protein functions on networks, we show that miRNAs predominantly act in a coordinated fashion to activate or repress signalling pathways responsible for metastatic traits in TNBC. We further demonstrate that our top candidate, miR-193b, regulates these phenotypes to an extent stronger than individual pathway inhibition, thus proving that its effect on TNBC aggressiveness is mediated by repressing multiple interconnected pathways.

cancer biology↗