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

Shi,Xiaohui; Cheng,Suisheng; Wang,Weixing

doi:10.3892/ol.2018.8496

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

Authors:
- Xiaohui Shi
- Suisheng Cheng
- Weixing Wang
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Affiliations: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China, Department of Thyroid Tumor Surgery, Tumor Center, Inner Mongolia Autonomous Region People's Hospital, Hohhot, Inner Mongolia 010000, P.R. China
Published online on: April 13, 2018 https://doi.org/10.3892/ol.2018.8496
Pages: 9202-9208
Copyright: © Shi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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.

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