CCT6A knockdown suppresses osteosarcoma cell growth and Akt pathway activation in vitro

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Weiquan Zeng1,2,3, Meizhu Wu2,3, Ying Cheng2,3

  • 1Department of Orthopaedics, Affiliated Rehabilitation Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.

Plos One
|December 30, 2022
PubMed

Insights

The protein-coding gene CCT6A is elevated in osteosarcoma. Silencing CCT6A inhibits cancer cell growth and survival, offering a potential therapeutic target for osteosarcoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Osteosarcoma is a primary bone cancer with limited treatment options.
  • The role of the chaperonin-containing TCP1 subunit 6A (CCT6A) gene in osteosarcoma remains uncharacterized.

Purpose of the Study:

  • To investigate the function of CCT6A in osteosarcoma.
  • To determine the effect of CCT6A knockdown on osteosarcoma cell behavior and molecular pathways.

Main Methods:

  • Analysis of CCT6A messenger RNA (mRNA) expression in osteosarcoma tissues and cells using the R2 genomic analysis tool.
  • Small interfering RNA (siRNA) mediated knockdown of CCT6A in cultured osteosarcoma cells.
  • Assessment of cell proliferation, viability, apoptosis, and cell cycle.
  • Western blot analysis to evaluate key protein expression levels (p-Akt, cyclinD1, Bcl-2, Bax).

Main Results:

  • CCT6A mRNA expression was significantly increased in osteosarcoma.
  • CCT6A knockdown led to reduced cell growth, viability, and survival.
  • Knockdown induced apoptosis and G0/G1 cell cycle arrest.
  • Downregulation of p-Akt, cyclinD1, and Bcl-2, with upregulation of Bax was observed following CCT6A knockdown.

Conclusions:

  • CCT6A plays a crucial role in promoting osteosarcoma cell proliferation and survival.
  • CCT6A knockdown inhibits tumor growth and induces apoptosis, partly through the Akt signaling pathway.
  • CCT6A represents a potential therapeutic target for osteosarcoma treatment.

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