SEPTIN3 Promotes Progression of Triple-Negative Breast Cancer via Activating Wnt Pathway

Abstract

Background

There is a lack of targeted therapies for triple-negative breast cancer (TNBC), necessitating the search for novel targets. Patients with TNBC exhibit elevated expression of neuron-specific septin-3 (SEPTIN3), leading to poor prognosis. This study aimed to investigate the modulation of SEPTIN3 expression in TNBC cells.

Methods

The relative expression levels of SEPTIN3 in TNBC tissues and cell lines were determined using Western blotting and qRT-PCR. We generated lentivirally transduced TNBC cell lines so such that SEPTIN3 was overexpressed or knocked down. Next, the effect of SEPTIN3 on the biological behavior of TNBC cells was detected using a series of functional assays, including CCK8, colony formation, scratch, and transwell assays. We monitored the tumorigenicity of SEPTIN3 overexpressed cells and performed Ki-67 immunostaining in mice. The mechanism mediated by SEPTIN3 was studied using functional enrichment analysis and Western blotting.

Results

Protein and mRNA expression levels of SEPTIN3 were observed to be increased in TNBC tissues and cell lines. SEPTIN3 knockdown reduced cell growth, invasion, and migration, whereas SEPTIN3 overexpression exerted the opposite effects. SEPTIN3 was observed to favor cell growth and tumorigenicity in vivo. In addition, SEPTIN3 promoted TNBC cell aggressiveness and proliferation via activation of the Wnt signaling pathway.

Conclusion

SEPTIN3 emerged as an oncogene that accelerates tumor progression by regulating the Wnt signaling pathway.

Keywords:

• triple-negative breast cancer
• SEPTIN3
• proliferation
• invasion
• Wnt signaling pathway

Data Sharing Statement

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Ethics Approval

All procedures performed were in accordance with the declaration of the ethical standards of the institutional research committee and with the Helsinki Declaration and its later amendments. The ethics committee has approved this study of the Huangshi Central Hospital.

Acknowledgments

We are very grateful for Huangshi Central Hospital for its help in this research.

Disclosure

All authors declare no conflicts of interest for this work.

Additional information

Funding

No funding was received.