# LncRNA PVT1 in human cancers: genomic complexity, isoforms, functional elements, mechanism of action, subcellular localization and possible role as a therapeutic target

## TL;DR

This review explores the role of the lncRNA PVT1 in cancer, covering its functions, mechanisms, and potential as a therapeutic target.

## Contribution

The paper introduces underexplored aspects of PVT1's subcellular localization and functional diversity in cancer.

## Key findings

- PVT1 has oncogenic roles but also notable exceptions in cancer biology.
- PVT1's subcellular localization varies across cancers and impacts its regulatory functions.
- PVT1 regulates gene expression through miRNA sponging and protein activity modulation.

## Abstract

PVT1 (Plasmacytoma Variant Translocation 1), a long non-coding RNA (lncRNA), is a critical player in diverse biological processes, particularly cancer biology. This review comprehensively examines PVT1’s multifaceted roles and molecular mechanisms. We delve into its predominant oncogenic functions while highlighting notable exceptions, offering new perspectives on its biological diversity. A key focus is the subcellular localizations of PVT1 across various cancers – an aspect underexplored in previous reviews despite its significant impact on function and regulatory mechanisms. Detailed mechanistic insights include PVT1’s linear and circular isoforms acting as miRNA sponges, its encoding of miRNAs, the influence of 8q24 rearrangements, and its regulation of protein stability/activity, and transcription. Furthermore, we examine PVT1’s functional elements, illuminating unexplored structural and regulatory features. The clinical implications of PVT1 as a biomarker and therapeutic target in oncology are also discussed. By synthesizing existing knowledge and introducing previously less-explored facets, this review aims to provide a comprehensive and up-to-date resource on PVT1’s role in health and disease.

The online version contains supplementary material available at 10.1186/s12943-026-02576-y.