The potential role of cofilin-1 in promoting triple negative breast cancer (TNBC) metastasis via the extracellular vesicles (EVs)

• Published in: Translational oncology 2022-01, Vol.15 (1), p.101247, Article 101247
• Main Authors: Howard, Jane, Goh, Chia Yin, Gorzel, Karolina Weiner, Higgins, Michaela, McCann, Amanda
• Format: Article
• Language: English
• Subjects: Cofilin-1; Extracellular vesicles; Liquid Biopsy; Metastasis; Review; Triple negative breast cancer
• ISSN: 1936-5233; 1936-5233
• DOI: 10.1016/j.tranon.2021.101247

•Triple negative breast cancer (TNBC) is a biological heterogeneous andn aggressive disease with a poor prognosis.•Extracellular vesicles have been shown to play a role in mediating metastasis.•Cofilin-1 has been detected in extracellular vesicles.•Cofilin-1 is involved in promoting triple negative breast cancer metastasis. Triple negative breast cancer (TNBC) is an aggressive cancer, particularly prone to metastasis and is associated with poor survival outcomes. The key to unravelling the aggressiveness of TNBC lies in decoding the mechanism by which it metastasises. Cofilin-1 is a well-studied member of the cofilin family, involved in actin depolymerisation. Studies have described the diverse roles of cofilin-1 including cell motility, apoptosis and lipid metabolism. Levels of cofilin-1 have been shown to be increased in many different types of malignant cells, with increased cofilin-1 protein levels associated with poor prognosis in patients with TNBC. Extracellular vesicles (EVs) are microvesicles typically around 100 nm in size, found in all biological fluids examined to date (Lötvall et al., 2014). Proteomic studies on extracellular vesicles (EVs) have shown that cofilin-1 is amongst the most frequently detected. Moreover, decreased levels of cofilin-1 potentially inhibit the release of EVs from cells. Additionally, Cofilin-1 is essential for the maturation of EVs and may also play a key role in the establishment of the pre-metastatic niche, thus promoting tumour cell migration. Further work into the exact mechanism by which cofilin-1 advances TNBC metastasis, may potentially prevent disease progression and improve outcomes for patients with TNBC. [Display omitted]