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Biology subjects

Voz, M. L.

Publications and source records attributed to Voz, M. L..

2 recordsLinked to original sources

Single-Cell Cross-Species Profiling identifies Conserved Transcriptional Networks in Early Pancreatic Tumourigenesis.

Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer and carries the poorest prognosis among all cancers, largely because it is frequently diagnosed at metastatic stages. It is therefore critical to identify reliable markers of preinvasive stages and to decipher the network driving preinvasive lesions to invasive carcinoma. Here, we generated a zebrafish model in which KRASG12D is specifically expressed in pancreatic acinar cells, inducing acinar-to-ductal metaplasia that faithfully mirrors mammalian tumorigenesis. Single cell RNA-seq allowed us to capture transcriptional changes occurring at early stages of the disease. Cross-species comparison with mouse and human scRNAseq transcriptomes revealed a striking conservation of the genes upregulated during metaplasia, triggering common signalling pathways and regulatory programs. Notably, metaplastic cells reactivate a broad set of developmental genes expressed in multipotent pancreatic progenitors. Mapping the acinar-to-cancer trajectories revealed a set of cytoskeletal and migration-related genes specifically upregulated during the late phase of metaplasia, immediately prior to malignant transformation, likely conferring invasive potential to these cells. SCENIC analysis further identified regulatory networks that become progressively activated as cells transition toward cancer, suggesting their involvement in the acquisition of malignant traits. In conclusion, our cross-species comparison demonstrates a high degree of conservation in the molecular mechanisms driving pancreatic cancer progression from early to late stages across evolutionarily distant species, including zebrafish, mouse, and human, highlighting critical pathways that should be targeted to prevent cancer progression. To allow researchers to easily explore gene expression profiles during pancreatic cancer progression across all three species, the datasets are publicly accessible via a user-friendly web platform (https://www.zddm.page.gd/)

cancer biology↗

A δ-cell subpopulation with a pro-β-cell identity confers efficient age-independent recovery in a zebrafish model of diabetes

Restoring damaged {beta}-cells in diabetic patients by harnessing the plasticity of other pancreatic cells raises the questions of the efficiency of the process and of the functionality of the new Insulin-expressing cells. To overcome the weak regenerative capacity of mammals, we used regeneration-prone zebrafish to study {beta}-cells arising following destruction. We show that most new insulin cells differ from the original {beta}-cells as they are Somatostatin+ Insulin+, but are nevertheless functional and normalize glycemia. These bihormonal cells are transcriptionally close to a subset of {delta}-cells in normal islets characterized by the expression of somatostatin 1.1 (sst1.1), the {beta}-cell genes pdx1, slc2a2 and gck, and the machinery for glucose-induced Insulin secretion. {beta}-cell destruction triggers massive sst1.1 {delta}-cell conversion to bihormonal cells. Our work shows that their pro- {beta}-cell identity predisposes this zebrafish {delta}-cell subpopulation to efficient age-independent neogenesis of Insulin-producing cells and provides clues to restoring functional {beta}-cells in mammalian diabetes models.

cell biology↗