Abstract
It has been proved that long noncoding RNAs (lncRNAs) are important modulators in the tumorigenesis and progression of various malignant tumors. Recently, lncRNA FOXD2-AS1 has been reported to be an oncogene in several kinds of human cancers. However, the function of FOXD2-AS1 in papillary thyroid cancer (PTC) has not been well investigated. This study aims to explore the biological role and mechanism of FOXD2-AS1 in PTC. At first, the expression of FOXD2-AS1 was examined in PTC tissues and cell lines with quantitative reverse transcription-polymerase chain reaction (qRT-PCR). FOXD2-AS1 was found to observably upregulated in PTC tissues and cell lines. Kaplan-Meier survival analysis revealed that high expression of FOXD2-AS1 was closely correlated with the unfavorable prognosis of patients with PTC. Based on the TCGA data set, KLK7 was overexpressed in PTC tumor samples. Our experimental data further validated the upregulation of KLK7 in PTC tissues and cell lines. Similarly, high level of KLKF was associated with poor prognosis of patients with PTC. The positive expression association between FOXD2-AS1 and KLK7 was analyzed with Pearson correlation coefficient. Loss-of-function assays revealed that knockdown of FOXD2-AS1 or KLK7 greatly inhibited PTC cell proliferation and migration, while induced cell apoptosis. Results of mechanism experiments suggested that FOXD2-AS1 functioned as a competing endogenous RNA (ceRNA) to enhance the expression of KLK7 by sponging miR-485-5p in PTC. Rescue assays were conducted to verify the function of FOXD2-AS1/miR-485-5p/KLK7 axis in PTC progression.
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