Open AccessIL‐34 is a potential biomarker for the treatment of papillary thyroid cancer
Author(s) -
Zhang Ping,
Zhang Hao,
Dong Wenwu,
Wang Zhihong,
Qin Yuan,
Wu Changhao,
Dong Qi
Publication year - 2020
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23335
Subject(s) - cancer research , mapk/erk pathway , apoptosis , oncogene , gene knockdown , thyroid carcinoma , transfection , flow cytometry , thyroid cancer , metastasis , blot , cancer , chemistry , biology , signal transduction , medicine , microbiology and biotechnology , cell cycle , thyroid , cell culture , endocrinology , biochemistry , genetics , gene
Background Interleukin (IL)‐34 is a recently discovered pro‐inflammatory cytokine and is a vital regulator in different tumor types. However, the function of IL‐34 in thyroid carcinoma has yet to be investigated. In this study, we analyzed the expression of IL‐34 in human papillary thyroid cancer (PTC) samples and determined its effects on the proliferation and apoptosis of PTC cells. Methods We examined the expression of IL‐34 in serum and tissue samples of patients with PTC by Western blotting and ELISA assay and analyzed its association with clinicopathological features including tumor size, tumor node metastasis (TNM) stage, and lymph node metastasis (LNM). We selected TPC1 and K1 for knockdown or overexpressing of IL‐34 via small interference RNA transfection. The proliferation of PTC cells was evaluated by CCK8 assay. We further investigated the role of IL‐34 in apoptosis by flow cytometry and studied the protein levels of epithelial‐mesenchymal transition (EMT) biomarkers, phosphorylated extracellular‐regulated kinase (ERK), and total‐ERK (t‐ERK) by Western blotting. Results Our results show that IL‐34 is significantly upregulated in serum and tissue samples from patients with PTC. IL‐34 promotes the proliferation and suppresses apoptosis in PTC cells. In addition, IL‐34 can promote the EMT and activate ERK signaling pathway in PTC cells. Conclusion This study provides novel evidence that IL‐34 serves as an oncogene in PTC. IL‐34 promotes proliferation, EMT phenotype, and ERK signaling pathway and inhibits apoptosis in PTC cells. Therefore, IL‐34 may be a potent therapeutic target for the treatment of PTC.