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Biology subjects

Poliani, P. L.

Publications and source records attributed to Poliani, P. L..

4 recordsLinked to original sources

Updating ACC preclinical models: characterization of two new patient-derived cell lines

AdrenoCortical Carcinoma (ACC) is an aggressive, rare and heterogenous malignancy, that requires diverse preclinical models. For this reason, the development of new cell lines is pivotal. Here we describe the development and characterization of two of them, SMAC-2 and SMAC-3, established from surgical specimens of ACC patients. The characterization included their mutational profiling, the evaluation of steroidogenic enzymes expression, secretory activity and the expression of steroid hormone receptors. The proliferative ability of these cells within a zebrafish embryos xenograft was also evaluated. SMAC-2 originated from a metastatic EDP-M-treated ACC in a female patient with Cushing syndrome and hyperandrogenism, while SMAC-3 derived from a male patient with a mitotane-treated local recurrence, with no sign of hypercortisolism. TP53 was mutated in both lines. SMAC-2 cells were characterized by a pathogenic alteration on CTTNB1 gene and a deletion of CDKN2A gene, while SMAC-3 on MSH2 gene. Basal hormonal status analysis showed a cell model-specific fingerprint either in the hormonal secretion and gene and protein expression of steroid hormone receptors. SMAC-2 secreted high levels of cortisol. SMAC-3 secreted low basal level of cortisol. Mitotane displayed in both cell lines a low potency. Under the experimental conditions used, the xenografted area did not increase for both cell models. Experiments were carried out to study the stability of the two cell lines. SMAC-2 and SMAC-3 display unique molecular and functional features, expanding the repertoire of experimental ACC models and representing valuable tools for preclinical research alongside established cell lines.

pharmacology and toxicology↗

Unveiling Oligodendrocyte-Lineage Differentiation in the Glioblastoma Infiltrative Zone Through Spatial Transcriptomics

IDH-wildtype glioblastoma (GBM) is the most aggressive primary brain tumor, characterized by limited therapeutic options and inevitable recurrence. This recurrence is driven by the highly infiltrative behavior of GBM cells, which prevents complete resection. Here, we performed spatially resolved transcriptomic profiling of four surgically defined GBM regions to characterize the infiltrative tumor compartment. Across multiple datasets and profiling approaches, the infiltrative zone showed reduced cellular heterogeneity compared with the tumor core. By comparison with an integrated reference of single-cell RNA sequencing data, we revealed that this reduction reflects a preferential differentiation of infiltrative GBM cells toward an oligodendrocyte-like lineage, accompanied by attenuated inflammatory signaling. In contrast, necrotic and proliferative regions display pronounced astrocyte-like and mesenchymal-like programs. Combined immunohistochemistry and fluorescence in situ hybridization confirmed the enrichment of oligodendrocyte-like tumor cells in the infiltrative area. Together, these findings identify the oligodendrocyte-like state as a defining feature and potential therapeutic vulnerability of infiltrative GBM driving brain invasion and relapse.

cancer biology↗

Expression of telomerase prevents ALT and maintains telomeric heterochromatin in juvenile brain tumors.

The activation of a telomere maintenance mechanism (TMM) is an essential step in cancer progression to escape replicative senescence and apoptosis. Paediatric brain tumors frequently exhibit Alternative Lengthening of Telomere (ALT) as active TMM, but the mechanisms involved in the induction of ALT in brain tumor cells are not clear.\n\nHere, we report a model of juvenile zebrafish brain tumor that progressively develops ALT. We discovered that reduced expression of tert and increase in Terra expression precedes ALT development. Additionally, tumors show persistent telomeric DNA damage and loss of heterochromatin marks at chromosome ends. Surprisingly, expression of telomerase reverts ALT features. Comparative analysis of gene expression after the rescue of ALT with telomerase and analysis of telomerase positive paediatric brain cancers showed increase of telomeric heterochromatin and maintenance of telomere length compared to ALT tumors, with reduced expression of genes of the pre-replicative complex as hallmark. Thus our study identifies telomere maintenance mechanisms as major drivers of telomeric DNA replication and chromatin status in brain cancers.

cancer biology↗

Altered function of the glutamate aspartate transporter GLAST in glioblastoma

In glioma patients, high levels of glutamate can cause brain edema and seizures. GLAST, a glutamate-aspartate transporter expressed by astrocytes with a role in glutamate uptake, is highly expressed on the plasma membrane of glioblastoma (GBM) cells, and its expression significantly correlates with shortened patient survival. Here, it was demonstrated that inhibition of GLAST expression limited the progression and invasion of GBM xenografts. Magnetic resonance spectroscopy was used to measure glutamate in GLAST-expressing gliomas showing that these tumors exhibit increased glutamate concentration. Despite their GLAST expression, GBM stem-like cells (GSCs) released rather than took up glutamate due to their lack of Na+/K+-ATPase. Overexpression of Na+/K+-ATPase in these cells restored glutamate uptake and induced apoptosis. The therapeutic relevance of targeting GLAST in gliomas was assessed using the inhibitor UCPH-101. In glioma-bearing mice, a single intratumoral injection of UCPH-101 significantly increased survival by decreasing GLAST expression and inducing apoptosis. Thus, GLAST has a novel role in GBM that appears to have crucial relevance in glutamate trafficking and may thus be a new therapeutic target.

cancer biology↗