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Published on: January 18, 2017
Epsin 3 potentiates the NF‑κB signaling pathway to regulate apoptosis in breast cancer
Qianxue Wu1, Qing Li1, Wenming Zhu1
1Department of Endocrine and Breast Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing 400016, P.R. China.
Abstract:
Endocrine drug resistance is common in some patients with estrogen receptor (ER)‑positive breast cancer, so it is necessary to identify potential therapeutic targets. The aim of the present study was to investigate the regulatory effect and mechanism of epsin 3 (EPN3) expression level changes on the proliferation and apoptosis of ER‑positive breast cancer. Online GEPIA was used to analyze the expression level of EPN3 in breast cancer. The online Kaplan‑Meier plotter tool was used to analyze the relationship between EPN3 expression and the prognosis of patients with breast cancer. Reverse transcription‑quantitative PCR, immunohistochemistry and western blotting were performed to detect the mRNA and protein expression levels of EPN3 in breast cancer tissues and cells. A lentiviral infection system was used to knockdown the expression of EPN3 in breast cancer cell lines. Cell Counting Kit‑8 and flow cytometry assays were conducted to detect the effect of EPN3 knockdown on breast cancer cell proliferation and apoptosis. Western blotting was used to detect the regulation of EPN3 expression on NF‑κB, and immunofluorescence was performed to detect the effect of EPN3 expression on NF‑κB nuclear translocation. The results demonstrated that the expression level of EPN3 in breast cancer tissues was higher compared with that in adjacent tissues (P<0.05). The expression level of EPN3 in the ER‑positive breast cancer cell line, MCF7, was higher compared with that in the other cell lines (MCF10A, ZR75‑1, MDA‑MB‑231, BT549 and SK‑BR‑3). After knocking down the expression of EPN3 in MCF7 cells, the proliferative ability of the cells was decreased, and the apoptosis rate was increased (P<0.05). After EPN3 knockdown in MCF7 cells, the phosphorylation of NF‑κB was decreased (P<0.05), and the nuclear translocation signal was weakened. Thus, it was suggested that EPN3 promoted cell proliferation and inhibited cell apoptosis by regulating the NF‑κB signaling pathway in ER‑positive breast cancer.
Insights
Epsinin 3 (EPN3) promotes ER-positive breast cancer growth and inhibits apoptosis by activating the NF-κB pathway. Targeting EPN3 may offer a new therapeutic strategy for endocrine drug resistance in breast cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Endocrine drug resistance is a significant challenge in treating estrogen receptor (ER)-positive breast cancer.
- Identifying novel therapeutic targets is crucial for improving patient outcomes.
- Epsinin 3 (EPN3) has emerged as a potential factor influencing cancer progression.
Purpose of the Study:
- To investigate the regulatory role of epsinin 3 (EPN3) expression in the proliferation and apoptosis of ER-positive breast cancer.
- To elucidate the underlying molecular mechanism of EPN3's action, particularly its effect on the NF-κB signaling pathway.
Main Methods:
- Bioinformatic analysis using GEPIA and Kaplan-Meier plotter for EPN3 expression and patient prognosis.
- Experimental validation of EPN3 mRNA and protein levels via RT-qPCR, immunohistochemistry, and Western blotting.
- Functional assays including EPN3 knockdown, cell proliferation (CCK-8), apoptosis (flow cytometry), and NF-κB pathway analysis (Western blotting, immunofluorescence).
Main Results:
- EPN3 expression was significantly upregulated in breast cancer tissues compared to adjacent tissues and was notably high in ER-positive MCF7 cells.
- Knockdown of EPN3 in MCF7 cells led to decreased proliferation and increased apoptosis.
- EPN3 knockdown suppressed NF-κB phosphorylation and nuclear translocation, indicating pathway inhibition.
Conclusions:
- Epsinin 3 (EPN3) promotes proliferation and inhibits apoptosis in ER-positive breast cancer.
- EPN3 exerts its effects by regulating the NF-κB signaling pathway.
- EPN3 represents a potential therapeutic target for overcoming endocrine drug resistance in ER-positive breast cancer.
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