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Interference with KCNJ2 inhibits proliferation, migration and EMT progression of apillary thyroid carcinoma cells by

Siyuan Chen1, Miaoming Huang2, Xiarong Hu1

  • 1The First Department of General Surgery, Affiliated Dongguan People's Hospital, Southern Medical University (Dongguan People's Hospital), Dongguan, Guangdong 523059, P.R. China.

Molecular Medicine Reports
|July 2, 2021
PubMed

Insights

Potassium inwardly rectifying channel subfamily J member 2 (KCNJ2) is upregulated in papillary thyroid carcinoma. Inhibiting KCNJ2 suppresses cancer cell proliferation, migration, and epithelial-mesenchymal transition by increasing G protein subunit γ2 (GNG2) expression.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Papillary thyroid carcinoma (PTC) is a prevalent endocrine malignancy.
  • The precise function and molecular mechanisms of potassium inwardly rectifying channel subfamily J member 2 (KCNJ2) in PTC are not well understood.

Purpose of the Study:

  • To investigate the role and molecular mechanism of KCNJ2 in papillary thyroid carcinoma.
  • To explore the relationship between KCNJ2 and G protein subunit γ2 (GNG2) in PTC progression.

Main Methods:

  • Gene Expression Profiling Interactive Analysis (GEPIA) database for KCNJ2 expression analysis.
  • Reverse transcription-quantitative PCR (RT-qPCR) and Western blot to detect KCNJ2 and GNG2 expression in PTC cell lines.
  • Cell transfection to inhibit KCNJ2 and GNG2 expression.
  • Colony formation, MTT, wound healing, and Transwell assays to assess cell proliferation, migration, and invasion.
  • Western blot to analyze protein expression related to transport and interstitial markers.

Main Results:

  • KCNJ2 expression was found to be significantly upregulated in papillary thyroid carcinoma tissues and cell lines.
  • Interference with KCNJ2 expression led to decreased proliferation, migration, and invasion of PTC cells.
  • KCNJ2 knockdown inhibited the epithelial-to-mesenchymal transition (EMT) process in PTC cells.
  • Upregulation of GNG2 expression was observed following KCNJ2 knockdown, suggesting a regulatory role.

Conclusions:

  • KCNJ2 plays a crucial role in promoting the proliferation, migration, and EMT of papillary thyroid carcinoma.
  • Interference with KCNJ2 effectively inhibits PTC progression, potentially through the upregulation of GNG2.
  • Targeting KCNJ2 could represent a novel therapeutic strategy for papillary thyroid carcinoma.
Keywords:
G protein subunit γ2epithelial‑to‑mesenchymal transitionmigrationpapillary thyroid carcinomapotassium inwardly rectifying channel subfamily J member 2proliferation

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