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Background <p>Perineural invasion (PNI) is a prevalent phenomenon in salivary adenoid cystic carcinoma (SACC). Nevertheless, the regulatory mechanism of PNI is largely elusive.</p> Methods <p>We detected Apolipoprotein D (ApoD) expression and further determined its role in SACC progression. Subsequently, the contributions of SACC-derived ApoD on neurite outgrowth of dorsal root ganglions (DRGs) cells were explored. Moreover, a series of in vivo assays were conducted to elucidate the role of ApoD in the SACC PNI process.</p> Results <p>We observed a dramatic up-regulation of ApoD in the SACC associated with an enhancement of PNI in patient biopsies. We found that SACC-derived ApoD elevated cancer cell migration and invasion. In addition, ApoD could facilitate the neurite outgrowth of cultured DRG cells in a CXCR4-dependent manner in vitro, as well as innervation, angiogenesis, and invasion along peripheral nerves of SACC in vivo. More importantly, by advanced bioinformatic analysis, we unexpectedly revealed a novel phenomenon ‘tumour cell to neuron-like cell transition’ in the ApoD-rich microenvironment in vivo, contributing to the neurogenesis in the SACC tumour.</p> Conclusion <p>we discovered a novel role of cancer-derived ApoD in the pathogenesis of PNI, which may represent an effective therapeutic target for SACC in clinics.</p>

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Apolipoprotein D is crucial for promoting perineural invasion in salivary adenoid cystic carcinoma

  • 期刊论文

  • 发表日期：

    2025年2月17日

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  • Guangzhao Huang,
  • Su Chen,
  • Bo Han,
  • Gaowei Zhang,
  • Mingzhe Bao,
  • Grace Paka Lubamba,
  • Yufei Hua,
  • Honglin Li,
  • Wenwen Liu,
  • Jiefei Shen,
  • Lei Wang,
  • Jie Lin,
  • Patrick Ming-Kuen Tang,
  • Zhangfan Ding,
  • Chunjie Li

摘要

Background

Perineural invasion (PNI) is a prevalent phenomenon in salivary adenoid cystic carcinoma (SACC). Nevertheless, the regulatory mechanism of PNI is largely elusive.

Methods

We detected Apolipoprotein D (ApoD) expression and further determined its role in SACC progression. Subsequently, the contributions of SACC-derived ApoD on neurite outgrowth of dorsal root ganglions (DRGs) cells were explored. Moreover, a series of in vivo assays were conducted to elucidate the role of ApoD in the SACC PNI process.

Results

We observed a dramatic up-regulation of ApoD in the SACC associated with an enhancement of PNI in patient biopsies. We found that SACC-derived ApoD elevated cancer cell migration and invasion. In addition, ApoD could facilitate the neurite outgrowth of cultured DRG cells in a CXCR4-dependent manner in vitro, as well as innervation, angiogenesis, and invasion along peripheral nerves of SACC in vivo. More importantly, by advanced bioinformatic analysis, we unexpectedly revealed a novel phenomenon ‘tumour cell to neuron-like cell transition’ in the ApoD-rich microenvironment in vivo, contributing to the neurogenesis in the SACC tumour.

Conclusion

we discovered a novel role of cancer-derived ApoD in the pathogenesis of PNI, which may represent an effective therapeutic target for SACC in clinics.