English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Breast cancer is a leading cause of cancer-associated mortality globally amongst gynecologic tumors due to aggressive metastasis. A previous study reported that neurensin-2 (NRSN2) was implicated in human cancer cells, and that NRSN2 gene and protein expression levels were significantly upregulated in human breast cancer tissues compared with adjacent non-tumor tissues. The purpose of the present study was to analyze the role of NRSN2 in the metastasis of breast cancer cells and explore its potential mechanism. Reverse transcription-quantitative PCR, MTT, western blotting and immunohistochemistry was used to analyze the role of NRSN2 both in vitro and in vivo . The present study demonstrated that NRSN2 knockdown inhibited the proliferation, migration and invasion of breast cancer cells in vitro . NRSN2 upregulation promoted breast cancer cell proliferation and tissue growth in vitro and in vivo . In addition, the results demonstrated that the regulatory effects of NRSN2 on breast cancer cells were associated with PI3K/AKT/mTOR and NF-κB signaling pathway dysregulation. Furthermore, NRSN2 overexpression in mice significantly promoted breast cancer cell proliferation. In conclusion, the results from the present study indicated that NRSN2 may be considered as a novel oncogenic protein and may represent a potential therapeutic target for breast cancer.

NRSN2 promotes breast cancer metastasis by activating PI3K/AKT/mTOR and NF‑κB signaling pathways