ArticleOncology research2017
Silencing of A-Kinase Anchor Protein 4 (AKAP4) Inhibits Proliferation and Progression of Thyroid Cancer.
Article in Oncology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Sex differences in thyroid aging and their implications in thyroid disorders: insights from gene regulatory networks.bioRxiv : the preprint server for biology · 2025Article
- LINC00511 influences cellular proliferation through cyclin-dependent kinases in papillary thyroid carcinoma.Journal of Cancer · 2020Article
- AKAP4, SPAG9 and NY-ESO-1 in Iranian Colorectal Cancer Patients as Probable Diagnostic and Prognostic BiomarkersAsian Pacific journal of cancer prevention : APJCP · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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