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ACAP3 negatively regulated by HDAC2 inhibits the malignant development of papillary thyroid carcinoma cells

Fenfen Zhan1, Ronghui Zhang2, Lanlan Qiu2

  • 1Endocrinology department, The Second Affiliated Hospital Zhejiang University School of Medicine, China; Endocrinology department, Sanmen People's Hospital, China.

The International Journal of Biochemistry & Cell Biology
|August 4, 2024
PubMed

Insights

Histone deacetylase 2 (HDAC2) negatively regulates ArfGAP with coiled-coil, ankyrin repeat and PH domains 3 (ACAP3) in papillary thyroid carcinoma (PTC). This interaction suppresses tumor proliferation and metastasis while promoting apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Papillary thyroid carcinoma (PTC) exhibits downregulated ArfGAP with coiled-coil, ankyrin repeat and PH domains 3 (ACAP3).
  • Histone deacetylase inhibitors (HDACIs) show therapeutic potential for PTC.
  • The relationship between histone deacetylase 2 (HDAC2) and ACAP3 in PTC requires investigation.

Purpose of the Study:

  • To investigate the potential relationship between HDAC2 and ACAP3 in papillary thyroid carcinoma.
  • To determine the functional impact of the HDAC2/ACAP3 axis on PTC cell behavior.
  • To elucidate the molecular mechanisms underlying ACAP3 regulation by HDAC2 in PTC.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) to assess ACAP3 and HDAC2 expression.
  • Pearson analysis to predict the correlation between HDAC2 and ACAP3.
  • Cellular assays (viability, proliferation, migration, invasion, apoptosis) and rescue experiments.
  • Western blot analysis for apoptosis-, epithelial-mesenchymal transition-, AKT-, and P53-related proteins.

Main Results:

  • ACAP3 was significantly downregulated in PTC tissues and cells.
  • ACAP3 overexpression suppressed PTC cell viability, proliferation, migration, and invasion, while promoting apoptosis.
  • HDAC2 overexpression reversed the tumor-suppressive effects of ACAP3, indicating a negative regulatory relationship.
  • HDAC2 negatively correlated with ACAP3 expression, affecting AKT and P53 signaling pathways.

Conclusions:

  • ACAP3 acts as a tumor suppressor in PTC by inhibiting proliferation and metastasis and facilitating apoptosis.
  • HDAC2 negatively regulates ACAP3, influencing key cellular processes in PTC.
  • Targeting the HDAC2/ACAP3 axis may offer a novel therapeutic strategy for papillary thyroid carcinoma.
Keywords:
ACAP3AKT pathwayApoptosisHistone deacetylase 2Papillary thyroid carcinoma

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