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Updated: Feb 10, 2026

Transoral Robotic Total Thyroidectomy and Bilateral Central Regional Lymph Node Dissection for Papillary Thyroid Carcinoma
Published on: September 15, 2023
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.
Abstract:
Papillary thyroid carcinoma (PTC) is the most frequently occurring subtype of thyroid cancer. A certain portion of PTCs can progress to recurrent metastatic cancer. Currently, there remains no effective molecular target therapy for PTCs. As a subunit of the chaperonin containing TCP1 (CCT) complex, CCT3 is involved in various biological processes. CCT3 has been reported to drive the proliferation of hepatocellular carcinoma cells. Nevertheless, it remains unknown whether CCT3 regulates the development of PTC. The present study examined CCT3 protein expression in 30 PTC samples from patients undergoing thyroidectomy. A significant increase was observed in CCT3 expression in the PTC samples compared with the matched adjacent normal thyroid tissues. Lentiviral-mediated small interfering RNAs were used to knock down CCT3 in K1 cells. It was observed that the expression of CCT3 was significantly suppressed in K1 cells infected with lentivirus containing a CCT3-targeting short hairpin RNA. Our results showed that CCT3 knockdown markedly decreased the proliferation and cell cycle progression of K1 cells. In addition, the knockdown of CCT3 induced apoptosis of K1 cell. Taken together, the findings of the present study indicated that CCT3 presents as a potential molecular marker of PTC and regulates the development of PTC in humans.
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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