Suppressed Krüppel‑like factor 17 expression induces tumor proliferation, metastasis and a poor prognosis in papillary thyroid carcinoma

Ye,Wen‑Chun; Gao,Li; Huang,Jing; Fang,Xiang‑Ming; Xie,Gang

doi:10.3892/mmr.2014.2429

October 2014 Volume 10 Issue 4

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October 2014 Volume 10 Issue 4

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Article

Suppressed Krüppel‑like factor 17 expression induces tumor proliferation, metastasis and a poor prognosis in papillary thyroid carcinoma

Authors:
- Wen‑Chun Ye
- Li Gao
- Jing Huang
- Xiang‑Ming Fang
- Gang Xie
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Affiliations: Department of Endocrinology, Mianyang Central Hospital, Mianyang, Sichuan 621000, P.R. China, Department of Pathology, Mianyang Central Hospital, Mianyang, Sichuan 621000, P.R. China
Pages: 2087-2092
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Published online on: July 29, 2014

https://doi.org/10.3892/mmr.2014.2429
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Abstract

Although the role of krüppel‑like factor 17 (KLF17) in the regulation of proliferation and epithelial‑mesenchymal transition has been examined in breast and liver cancer, their effect on papillary thyroid carcinoma (PTC) remains to be elucidated. The present study aimed to investigate the expression pattern of KLF17 in PTC and the correlation between KLF17 expression and the malignant potential of PTC. KLF17 expression in PTC and adjacent liver tissues was studied by polymerase chain reaction and western blot analysis, and the association between KLF17 expression and the clinicopathological features of PTC was studied in 50 patients. By using RNA interference against KLF17, the correlation between KLF17 expression and malignant potential was examined by downregulating KLF17 expression in TPC‑1 cells, and the effects of KLF17 downregulation on cell proliferation and motility were analyzed. Furthermore, the association between KLF17 expression and the surgical outcomes of PTC patients were analyzed. Downregulated expression of KLF17 was associated with a shorter overall survival time in clinical patients (P<0.05). Low KLF17 expression was significantly associated with tumor stage, tumor size, nodal stage and metastasis stage in PTC (P<0.05). The reduced expression of KLF17 promoted the motility and proliferation ability of TPC‑1 cells by altering the expression of tight junction protein 1 and Snai1, and activating the AKT pathway by upregulating inhibitor of DNA binding 1. In conclusion, the present study demonstrated that KLF17 is important in tumor proliferation and may be a useful prognostic indicator in directing therapy. Therefore, further investigation regarding the role of KLF17 in PTC is required.

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