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Petruzzelli, R.

Publications and source records attributed to Petruzzelli, R..

2 recordsLinked to original sources

De novo Golgi biogenesis requires coordinated transactivation of a Golgi regulon

The Golgi apparatus expands during differentiation and high secretory demand, yet the transcriptional control of its biogenesis remains poorly defined. Here, we developed a targeted enzymatic ablation method to eliminate the Golgi and trigger de novo organelle formation. Single-cell RNA-seq of cells rebuilding Golgi revealed an orchestrated induction of a broad Golgi gene network coinciding with structural and functional organelle maturation. This gene set spans all Golgi sub-compartments and functions, including glycosylation, trafficking, and ion transport, thus supporting the concept of a unified Golgi regulon, enabling the simultaneous expression of components required for the organelle structural and functional integrity. Through promoter analysis and RNAi screening, we identified CREB3L1 as a key transcriptional regulator critical for Golgi gene activation and organelle reformation. These findings indicate that CREB3L1-dependent transcriptional mechanisms orchestrate a complete Golgi biogenesis program that may be essential for organelle regeneration and for secretory pathway plasticity during physiological remodeling.

cell biology↗

Synthetic lethality screening reveals FDA-approved drugs that overcome ATP7B-mediated tolerance of tumor cells to cisplatin

Tumor resistance to chemotherapy represents an important challenge in modern oncology. Although platinum (Pt)-based drugs have demonstrated excellent therapeutic potential, their effectiveness in a wide range of tumors is limited by the development of resistance mechanisms. One of these mechanisms includes increased cisplatin sequestration/efflux by the copper-transporting ATPase, ATP7B. However, targeting ATP7B to reduce Pt tolerance in tumors could represent a serious risk because suppression of ATP7B might compromise copper homeostasis, as happens in Wilson disease.\n\nTo circumvent ATP7B-mediated Pt tolerance we employed a high-throughput screen (HTS) of an FDA/EMA-approved drug library to detect safe therapeutic molecules that promote cisplatin toxicity in the resistant ovarian carcinoma cell line IGROV-CP20. Using a synthetic lethality approach we identified and validated three hits (Tranilast, Telmisartan and Amphotericin B) that could reduce cisplatin resistance. All three drugs induced Pt-mediated DNA damage and inhibited either expression or trafficking of ATP7B in a tumor-specific manner. Global transcriptome analyses showed that Tranilast and Amphotericin B affect expression of genes operating in several pathways that confer tolerance to cisplatin. In the case of Tranilast, these included key molecular players operating in the distribution of platinum to different intracellular compartments. In particular, Tranilast was found to suppress ATOX1 and, as a consequence, ATOX1-mediated trafficking of ATP7B in response to cisplatin.\n\nConsidering the well-known safety profiles of Tranilast, Telmisartan and Amphotericin B, these drugs emerge as potential candidates that might be used for the rapid development of new therapeutic strategies to overcome resistance of tumors to Pt-based chemotherapy.

cancer biology↗