The silencing of FNDC1 inhibits the tumorigenesis of breast cancer cells via modulation of the PI3K/Akt signaling pathway
- Chen Yunwen
- Gao Shanshan
- Ben Zhifei
- Chen Saijun
- Yin Hua
Affiliations: Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China
- Published online on: April 22, 2021 https://doi.org/10.3892/mmr.2021.12118
Copyright: © Yunwen
et al. This is an open access article distributed under the
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Fibronectin type III domain‑containing protein 1 (FNDC1) is a protein that contains a major component of the structural domain of fibronectin. Although many studies have indicated that FNDC1 serves vital roles in the development of various diseases, the role of FNDC1 in the progression of breast cancer (BC) remains elusive. The aim of the present study was to investigate the biological functions of FNDC1 in BC cells and the associated mechanisms. The expression levels of FNDC1 in BC tissues and normal breast tissues were analyzed using The Cancer Genome Atlas database (TCGA). Kaplan‑Meier curves were mined from TCGA to examine the clinical prognostic significance of FNDC1 mRNA in patients with BC. The expression of FNDC1 was knocked down by transfection with shRNA in BC cells. Cell viability, colony formation ability, migration and invasion were assayed following the silencing of FNDC1 in BC cells. The expression of proteins was measured using a western blotting assay. The bioinformatic data indicated that the FNDC1 mRNA expression levels were significantly upregulated in BC tissues compared with normal breast tissues, and the high mRNA expression levels of FNDC1 were associated with a lower overall survival in patients with BC. The downregulation of FNDC1 inhibited the proliferation, colony formation, migration and invasion of BC cells. Investigation of the mechanisms revealed that the silencing of FNDC1 decreased the protein expression levels of MMPs and epithelial‑to‑mesenchymal markers. Furthermore, the silencing of FNDC1 led to the inactivation of the PI3K/Akt signaling pathway. FNDC1 was highly upregulated and acted as an oncogene in BC. Therefore, targeting FNDC1 may be a potential strategy for the treatment of BC.