# Inhibition of NR2F2 suppresses invasion ability and modulates EMT marker in head and neck squamous cell carcinoma

## TL;DR

This study shows that inhibiting NR2F2 reduces cancer cell invasion and changes EMT markers in head and neck squamous cell carcinoma.

## Contribution

The study identifies NR2F2 as a potential therapeutic target in HNSCC by demonstrating its role in invasion and EMT modulation.

## Key findings

- NR2F2 inhibition significantly decreases invasion and migration of HNSCC cells.
- NR2F2 inhibition modulates epithelial-mesenchymal transition (EMT) markers in HNSCC cells.
- NR2F2 expression is upregulated in HNSCC patients with lymph node metastasis.

## Abstract

The nuclear receptor subfamily 2 group F member 2 (NR2F2) has emerged as a potential therapeutic target in cancer due to its involvement in tumor progression, metastasis, angiogenesis, and epithelial-mesenchymal transition (EMT). However, its precise role in head and neck squamous cell carcinoma (HNSCC) and other cancer types remains to be elucidated. To investigate the role of NR2F2 in HNSCC, we examined its expression in relation to lymph node metastasis (LNM) in patient samples. Further functional studies were conducted using knockdown experiments and NR2F2 inhibitors, COUP-TFII inhibitor A(CIA) and 4-methoxynaphthalene-1-ol(4-MNol), in HNSCC cell lines. Invasion and migration assays were performed to assess the impact of NR2F2 modulation. Additionally, Western blot analysis was conducted to investigate the effect of NR2F2 inhibition on epithelial-mesenchymal transition (EMT) markers. NR2F2 expression was found to be upregulated in HNSCC patients with LNM, suggesting its involvement in tumor progression and metastasis. Knockdown of NR2F2 significantly decreased the invasion and migration of HNSCC cells. Inhibition of NR2F2 using CIA and 4-MNol also resulted in reduced invasion ability and modulation of EMT markers in HNSCC cells.

This study highlights the significance of NR2F2 in HNSCC and provides evidence for its role in promoting the invasion and migration of cancer cells. The findings suggest that NR2F2 may serve as a potential therapeutic target in HNSCC and other cancer types. Further research and development of NR2F2-targeted therapies are warranted for improved treatment strategies in cancer patients.

The online version contains supplementary material available at 10.1007/s12672-025-03539-3.