Thyroid cancer is one of the most common malignancies of the endocrine system. The incidence of thyroid cancer has continued to rise in the past several decades worldwide [
1]. In 2013, there were 143,900 new cases of thyroid cancer reported and 6500 deaths in China, the national incidence of thyroid cancer was 10.58 per 100,000 (5.12 per 100,000 for men and 16.32 per 100,000 for women), and the ratio between males and females was 1:3.2 [
2]. Thyroid papillary carcinoma is the most common type and contributes to more than 85% of thyroid cancer [
3]. Previous studies have established that excessive activation of the MAPK pathway can drive carcinogenesis in BRAF, RAS, and RET gene mutation induced by PTC, and activator protein-1 (AP-1) is an important target of the MAPK pathway [
4,
5].
AP-1 is a leucine zipper protein dimer that is composed of Jun (c-Jun, JunB, and JunD), Fos (c-Fos, FosB, Fra-1, and Fra-2), ATF (ATF-2, LRF1/ATF-3, B-ATF), JDP (JDP-1, JDP-2), and Maf (c-Maf, MafA, MafB, MafG/F/K, Nrl) [
6]. Jun protein is able to form homodimer by itself; it also can form heterodimer with Fos and ATF protein family members. However, Fos protein cannot form homodimer with Jun protein. Jun-Fos dimer is the most common form of AP-1 protein in human cells. AP-1 is a downstream transcription factor of the MAPK signaling pathway that binds to specific DNA sequences on other genes, participating in a wide range of cellular processes, including cell growth, differentiation, and apoptosis [
7]. Growth factors, neurotransmitters, cytokine, stress, ultraviolet, and other physiological factors can activate the transcription factor AP-1 via the MAPK signaling pathway and increase the transcriptional activity of Jun and Fos. The post-transcriptional phosphorylation and dephosphorylation of Jun and Fos can regulate the process of cell proliferation, invasion, metastasis, survival, and apoptosis [
8]. When AP-1 is inappropriately expressed, it is closely related to pathological processes such as tumor cell transformation, angiogenesis, metastasis, immunity, and inflammatory diseases [
9,
10]. It has been shown that nasopharyngeal cancer tissues have increased expression of AP-1 compared with normal tissues, and it was related to the progression of tumor cells [
11]. Blocking the transcriptional activation of AP-1 suppresses the process of breast cancer cell invasion [
12]. Some studies have also reported that the expression of AP-1 protein is upregulated in various tumor tissues such as pancreatic cancer [
13] and colon cancer [
14]. However, the mechanisms of AP-1 and papillary thyroid carcinoma are not well studied. The purpose of our study is to evaluate the expression and clinical significance of AP-1 in papillary thyroid carcinoma.