The role of circular RNAs in cancer has started to be deeply investigated in order to identify new molecular targets for future personalized anti tumoral therapies. Here, we investigated the pivotal role of a peculiar circRNA called circPVT1 demonstrating for the first time that it is able to act as miRNA sponge for the well-known metabolic miRNA, miR-33a-5p leading to the upregulation of its targets among them c-Myc, located in the same locus of PVT1 gene. Previous studies showed that c-Myc could regulate indirectly through miRNAs expression Glutaminase, the first enzyme involved in glutaminolysis, the metabolic pathway deregulated in breast cancer. Notably, we demonstrated for the first time that c-Myc acts as transcriptional factor directly regulating Glutaminase expression. These data provide new insights about the role of non-coding RNAs as upstream regulators of cell metabolism which contributes to cancer onset and progression.

CircPVT1 as non coding mediator of breast cancer metabolism / Palcau, ALINA CATALINA. - (2024 Jan 29).

CircPVT1 as non coding mediator of breast cancer metabolism

PALCAU, ALINA CATALINA
29/01/2024

Abstract

The role of circular RNAs in cancer has started to be deeply investigated in order to identify new molecular targets for future personalized anti tumoral therapies. Here, we investigated the pivotal role of a peculiar circRNA called circPVT1 demonstrating for the first time that it is able to act as miRNA sponge for the well-known metabolic miRNA, miR-33a-5p leading to the upregulation of its targets among them c-Myc, located in the same locus of PVT1 gene. Previous studies showed that c-Myc could regulate indirectly through miRNAs expression Glutaminase, the first enzyme involved in glutaminolysis, the metabolic pathway deregulated in breast cancer. Notably, we demonstrated for the first time that c-Myc acts as transcriptional factor directly regulating Glutaminase expression. These data provide new insights about the role of non-coding RNAs as upstream regulators of cell metabolism which contributes to cancer onset and progression.
29-gen-2024
Giovanni Blandino
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1706077
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