Open Access
Silencing of A-Kinase Anchor Protein 4 (AKAP4) Inhibits Proliferation and Progression of Thyroid Cancer
Author(s) -
Jiakai Han,
Wei Gao,
Daizhong Su,
Yang Liu
Publication year - 2017
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504016x14783701102564
Subject(s) - gene knockdown , cancer research , thyroid cancer , biology , gene silencing , metastasis , cell growth , thyroid , downregulation and upregulation , cancer cell , cancer , cell culture , endocrinology , genetics , gene
A-kinase anchor protein 4 (AKAP4), a member of the A-kinase anchor family of proteins, plays a role in tumor development and progression. However, its expression pattern and function in human thyroid cancer remain obscure. Here we examined AKAP4 expression in thyroid cancer cell lines as well as the effects of AKAP4 on the proliferation and metastasis of thyroid cancer cells. We also explored the molecular mechanism by which AKAP4 mediates the metastatic potential of thyroid cancer cells. Our results revealed that the transcript and protein levels of AKAP4 were significantly upregulated in thyroid cancer cell lines. In vitro experiments showed that knockdown of AKAP4 significantly inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process in thyroid cancer cells. Additionally, knockdown of AKAP4 greatly decreased the protein expression of Shh as well as Smo, Ptc, and Gli-1 in ACT-1 cells. Finally, the in vivo nude mice model confirmed that knockdown of AKAP4 attenuated tumor growth. In conclusion, our findings demonstrated that knockdown of AKAP4 inhibited proliferation and metastasis, likely through suppressing the Shh signaling pathway, in thyroid cancer cells. Thus, AKAP4 may act as a potential therapeutic target for human thyroid cancer.