# Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers

## TL;DR

BST2 is a molecule that plays roles in cancer growth and immune evasion, making it a potential target for cancer treatment.

## Contribution

The paper reveals BST2's dual role as an oncogenic driver and immunoregulatory hub in various cancers.

## Key findings

- BST2 promotes cancer cell proliferation and resistance to stress.
- BST2 influences the tumor microenvironment by affecting immune cells.
- High BST2 levels correlate with poor outcomes in several cancers.

## Abstract

BST2 has emerged as a multifunctional molecule that bridges antiviral defense, membrane architecture, and tumor immunity. Originally characterized as an interferon-inducible restriction factor that tethers virions to the plasma membrane, BST2 is now recognized as an oncogenic driver and immunoregulatory hub in diverse malignancies. In cancer, BST2 expression is frequently upregulated through promoter hypomethylation and transcriptional activation. Functionally, BST2 promotes proliferation, epithelial–mesenchymal transition, anoikis resistance, and chemoresistance, whereas its loss sensitizes tumor cells to proteotoxic and metabolic stresses. Beyond tumor cells, BST2 modulates the tumor microenvironment by promoting M2 macrophage infiltration, dendritic cell exhaustion, and natural killer (NK)-cell resistance, thereby contributing to immune evasion. Elevated BST2 expression correlates with poor prognosis in glioblastoma, breast, nasopharyngeal, and pancreatic cancers, and it serves as a circulating biomarker within small extracellular vesicles. In conclusion, BST2 is a dual-function molecule that integrates oncogenic signaling and immune regulation, making it an attractive diagnostic and therapeutic target for hematological and solid tumors.