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HPGD Inhibited Natural Killer Cell Activation and Enhanced Autophagy to Promote the Progression of Papillary Thyroid

Jinfeng Lou1, Yong Luo2, Jiahui Yang2

  • 1Department of Anesthesiology, Ningbo Medical Center Lihuili Hospital, Ningbo 315040, Zhejiang, P.R. China.

Current Cancer Drug Targets
|May 15, 2026
PubMed
Abstract

Insights

This study reveals that high HPGD expression promotes papillary thyroid cancer (PTC) by activating autophagy and JAK2/STAT3 signaling, while suppressing natural killer cell activity. Targeting HPGD may offer a new therapeutic strategy for PTC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • The role of Hydroxyprostaglandin dehydrogenase (HPGD) in papillary thyroid cancer (PTC) is not well understood.
  • HPGD is known to be involved in various cancers, but its specific function in PTC requires investigation.

Purpose of the Study:

  • To investigate the role of HPGD in PTC.
  • To elucidate the underlying mechanisms of HPGD action in PTC, including its impact on cell behavior and the tumor immune microenvironment.

Main Methods:

  • Analysis of HPGD expression in PTC using TCGA data.
  • Kaplan-Meier survival and ROC analyses for prognostic and diagnostic value assessment.
  • In vitro functional experiments (knockdown/overexpression) in TPC-1 cells to assess proliferation, migration, invasion, autophagy, and JAK/STAT signaling.
  • Tumor immune microenvironment (TIME) analysis and evaluation of HPGD's effect on natural killer (NK) cell cytotoxicity.

Main Results:

  • High HPGD expression correlates with poor prognosis in PTC.
  • HPGD overexpression enhances PTC cell proliferation, migration, and invasion, while knockdown inhibits these processes.
  • HPGD activates autophagy and the JAK2/STAT3 pathway, suppresses NK cell cytotoxicity by reducing ICAM-1, and alters TIME by increasing immune and stromal scores.

Conclusions:

  • HPGD plays a tumor-promoting and immune-suppressive role in PTC, distinct from its role in other cancers.
  • HPGD's mechanism involves regulating autophagy, JAK2/STAT3 signaling, and NK cell cytotoxicity in a cancer-type-specific manner.
  • Targeting HPGD presents a potential therapeutic strategy for PTC.
Keywords:
15-hydroxyprostaglandin dehydrogenaseJak/stat3 activationPapillary thyroid cancerautophagy.mechanismnatural killer cellstumor immune microenvironments

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