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Oncol Lett. 2019 Mar;17(3):2969-2975. doi: 10.3892/ol.2019.9937. Epub 2019 Jan 15.

NDNF inhibits the migration and invasion of human renal cancer cells through epithelial-mesenchymal transition.

Xia L1,2, Li S1,2, Liu Y1,2,3, Huang Y1,2, Ni B1,2, Wan L1,2,3, Mei H1,2, Li X4, Cai Z1,2, Li Z1,2.

Author information

1
Guangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong 518000, P.R. China.
2
Shenzhen Key Laboratory of Genitourinary Tumor, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong 518000, P.R. China.
3
Department of Oncology, Guangzhou Medical University, Guangzhou, Guangdong 510182, P.R. China.
4
Department of Urology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, P.R. China.

Abstract

Neuron-derived neurotrophic factor (NDNF) is a glycosylated, disulfide-bonded secretory protein that contains a fibronectin type III domain. NDNF has been identified as a neurotrophic factor; however, its role in carcinogenesis has not yet been identified. To investigate the expression and role of NDNF in carcinogenesis, the expression of NDNF in human Renal cell carcinoma (RCC) cell lines and tissues was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. Cell proliferation was investigated using CCK-8 and colony formation assays, and the cell invasion and immigration capacity was evaluated using the transwell assay. The results demonstrated that NDNF expression was downregulated in RCC cell lines and RCC tissues. Restoring NDNF expression significantly inhibited the proliferation, migration and invasion of RCC cells. The study also demonstrated that the inhibitory effect of NDNF on invasive ability was mediated by suppressing the epithelial-mesenchymal transition (EMT) in RCC cells. NDNF may therefore be considered an important regulator of EMT in RCC progression and may represent a novel promising target for antimetastatic therapy.

KEYWORDS:

EMT; NDNF; RCC; invasion; migration

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