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<p>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.</p><p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月15日

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  • Joo Kyung Noh,
  • Seon Rang Woo,
  • Min Kyeong Lee,
  • Jung Woo Lee,
  • Young Chan Lee,
  • Seong-Gyu Ko,
  • Young-Gyu Eun

摘要

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.