Knockdown of eIF3a attenuated cell growth in K1 human thyroid cancer cells

Xucai Zheng1, Shengying Wang2, Shikai Hong1

  • 1Department of Head and Neck, Breast Surgery, the First Affiliated Hospital of University of Science and Technology of China, Anhui Provincial Cancer Hospital, No.107 Huanhu East Road, Hefei, 230001, China.

Genes & Genomics
|February 17, 2021
PubMed
Abstract

Insights

Eukaryotic translation initiation factor 3a (eIF3a) promotes thyroid cancer cell proliferation and is linked to tumor grade. Inhibiting eIF3a reduces proliferation and increases apoptosis, suggesting it as a potential gene therapy target.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Eukaryotic translation initiation factor 3a (eIF3a) is a key subunit of the eIF3 complex, crucial for ribosome establishment and translation initiation.
  • Abnormal eIF3a expression is implicated in the tumorigenesis of various cancer types.

Purpose of the Study:

  • To investigate the role of eIF3a in human thyroid cancer (TC).

Main Methods:

  • eIF3a expression was quantified in TC tissues and cell lines using qRT-PCR and immunohistochemistry.
  • Functional assays including cell proliferation, cell cycle, and apoptosis were performed after eIF3a knockdown in K1 cells.

Main Results:

  • eIF3a mRNA levels were elevated in TC tissues and cancer cell lines, correlating with higher tumor grade.
  • eIF3a knockdown significantly inhibited cell proliferation, induced apoptosis, and caused cell cycle arrest at S and G2/M phases in K1 cells.
  • Downregulation of phosphorylated ERK1/2 and survivin was observed post eIF3a knockdown.

Conclusions:

  • eIF3a significantly contributes to thyroid cancer cell proliferation.
  • eIF3a represents a potential therapeutic target for gene therapy in human thyroid cancer.