Suppression of CCT3 inhibits malignant proliferation of human papillary thyroid carcinoma cell

Xiaohui Shi1, Suisheng Cheng2, Weixing Wang1

  • 1Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Oncology Letters
|May 29, 2018
PubMed

Insights

Chaperonin-containing TCP1 subunit 3 (CCT3) is upregulated in papillary thyroid carcinoma (PTC). Silencing CCT3 inhibits PTC cell proliferation and induces apoptosis, suggesting CCT3 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Papillary thyroid carcinoma (PTC) is the most common thyroid cancer subtype, with limited targeted therapies for recurrent or metastatic disease.
  • The chaperonin-containing TCP1 (CCT) complex subunit CCT3 is implicated in hepatocellular carcinoma proliferation, but its role in PTC is unelucidated.

Purpose of the Study:

  • To investigate the expression and function of CCT3 in papillary thyroid carcinoma.
  • To determine if CCT3 could serve as a potential molecular marker or therapeutic target for PTC.

Main Methods:

  • CCT3 protein expression was quantified in 30 PTC samples and adjacent normal tissues using immunohistochemistry.
  • CCT3 was knocked down in PTC K1 cells using lentiviral-mediated short hairpin RNA (shRNA).
  • Cell proliferation, cell cycle progression, and apoptosis were assessed after CCT3 knockdown.

Main Results:

  • CCT3 expression was significantly elevated in PTC tissues compared to normal thyroid tissues.
  • CCT3 knockdown in K1 cells led to a marked reduction in cell proliferation and cell cycle progression.
  • Downregulation of CCT3 induced apoptosis in K1 cells.

Conclusions:

  • CCT3 is overexpressed in papillary thyroid carcinoma.
  • CCT3 plays a crucial role in regulating PTC cell proliferation, cell cycle, and apoptosis.
  • CCT3 represents a potential molecular marker and therapeutic target for PTC.

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