KPNA4 regulated by miR-548b-3p promotes the malignant phenotypes of papillary thyroid cancer.

AIM:Karyopherin α4 importin α3) has been verified to be an oncogene in many cancers. However, its role in papillary thyroid cancer (PTC), the most frequent endocrine malignancy, is still unclear. MATERIALS AND expression was analyzed in PTC tissues and cells. The effects of on the proliferation, invasion, and apoptosis of PTC cells were evaluated after overexpression or downregulation of The influence of Kduanyu15354 on NF-κB activation was evaluated by nuclear NF-κB p65 expression and NF-κB-luciferase reporter assays. Moreover, we also explored whether Kduanyu15354 was regulated by miR-548b-3p. Additionally, the roles of miR-548b-3p and Kduanyu15354 were explored in a xenograft mouse model. KEY expression was increased in PTC tissues and cells, and its expression was significantly related to patients' clinicopathologic features and overall survival. Overexpression of Kduanyu15354 significantly promoted PTC cell proliferation and invasion, enhanced nuclear p65 expression and augmented NF-κB luciferase activity. However, Kduanyu15354 silencing showed opposite effects on the above indexes, and induced apoptosis of PTC cells. Kduanyu15354 was a target of miR-548b-3p, which was downregulated in PTC and inhibited proliferation and invasion, but promoted apoptosis of PTC cells. Kduanyu15354 overexpression abrogated the suppression of miR-548b-3p on the malignant phenotypes of PTC cells. Both miR-548b-3p overexpression and Kduanyu15354 downregulation inhibited tumor growth and Ki-67 expression, elevated numbers of Tunel-positive cells, and deceased nuclear p65 expression in mouse tumor was negatively regulated by miR-548b-3p and promoted the development of PTC via activating the NF-κB pathway.

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