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Silencing of TCTN1 inhibits proliferation, induces cell cycle arrest and apoptosis in human thyroid cancer.

Silencing of TCTN1 inhibits proliferation, induces cell cycle arrest and apoptosis in human thyroid cancer.
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Xu P, Xia X, Yang Z, Tian Y, Di J, Guo M,


Xu P, Xia X, Yang Z, Tian Y, Di J, Guo M, (click to view)

Xu P, Xia X, Yang Z, Tian Y, Di J, Guo M,

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Experimental and therapeutic medicine 2017 08 1614(4) 3720-3726 doi 10.3892/etm.2017.4940

Abstract

Tectonic family member 1 (TCTN1) is one of the tectonic family members, and a regulator of the hedgehog signaling pathway, which has been studied in various cancer types, including prostate and pancreatic cancer. However, its function in thyroid cancer has not been well documented. Therefore, the present study investigated the function of TCTN1 in thyroid cancer using a loss-of-function assay. Lentivirus-mediated RNA interference was applied to downregulate TCTN1 in the thyroid cancer cell lines, CAL62 and 8305C. A series of functional properties, including cell viability, colony formation, cell cycle and apoptosis were determined using MTT, colony formation assay and flow cytometry analyses, respectively. The results demonstrated that lentivirus-medicated RNAi could specifically suppress the expression of TCTN1 at the mRNA and protein levels in CAL62, and 8305C cells. Knockdown of TCTN1 inhibited cell growth and proliferation via inducing S phase arrest, and apoptosis. Mechanistically, the S phase arrest was accompanied by the upregulation of cyclin dependent kinase 2, cyclin A2 and downregulation of cyclin B1. Knockdown of TCTN1 induced apoptosis through increasing the expression of Bcl2-associated agonist of cell death, cleaved caspase-3 and poly(ADP-ribose)polymerase, and decreasing apoptosis regulator Bcl-2 expression. The current study highlights the essential role of TCTN1 in promoting thyroid cancer cell proliferation, and its knockdown may serve as a potential therapeutic treatment for thyroid cancer.

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