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Down-regulated FST expression is involved in the poor prognosis of triple-negative breast cancer
Sainan Liu1, Bin Liu2, Qian Zhao1
1Department of Epidemiology and Biostatistics, School of Public Health, Jilin University, Changchun, 130021, China.
Background:
Triple-negative breast cancer (TNBC) is more commonly associated with young patients, featuring high histological grade, visceral metastasis, and distant recurrence. Follistatin (FST) is a secreted extracellular regulatory protein that antagonizes TGF-β superfamily such as activin and TGF-β related superfamily such as bone morphogenetic protein (BMP). The implication of FST in the proliferation, angiogenesis, and metastasis of solid tumors documents good or poor outcome of patients with BC. However, the role of FST in TNBC remains unclear.
Methods:
Data of 935 patients with breast cancer (BC) were extracted from TCGA. Case-control study, Kaplan-Meier, uni-multivariate COX, and ROC curve were utilized to investigate the relationship between FST expression and the clinical characteristics and prognosis of BC. Functional studies were used to analyze the effect of FST expression on proliferation, apoptosis, migration, and invasion of TNBC cell lines. Bioinformatic methods such as volcanoplot, GO annd KEGG enrichment, and protein-protein interactions (PPI) analyses were conducted to further confirm the different roles of FST in the apoptotic pathways among mesenchymal and mesenchymal stem-like cells of TNBC.
Results:
Data from TCGA showed that low FST expression correlated with poor prognosis (for univariate analysis, HR = 0.47, 95% CI: 0.27-0.82, p = 0.008; for multivariate analysis, HR = 0.40, 95% CI: 0.21-0.75, p = 0.004). Low FST expression provided high predicted value of poor prognosis in TNBC amongst BCs. FST knockdown promoted the proliferation, migration and invasion of BT549 and HS578T cell lines. FST inhibited the apoptosis of mesenchymal cells by targeting BMP7.
Conclusions:
Low FST expression is associated with poor prognosis of patients with TNBC. FST expressions exhibit the anisotropic roles of apoptosis between mesenchymal and mesenchymal stem-like cells but promote the proliferation, migration, invasion in both of two subtypes of TNBC in vitro. FST may be a subtype-heterogeneous biomarker for monitoring the progress of TNBC.
Insights
Low follistatin (FST) expression correlates with poor prognosis in triple-negative breast cancer (TNBC). FST knockdown promotes TNBC cell proliferation and invasion, suggesting FST as a potential biomarker.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Triple-negative breast cancer (TNBC) presents aggressive clinical features and poor outcomes.
- Follistatin (FST), a regulator of TGF-β superfamily, has implications in various solid tumors, but its role in TNBC is not well-defined.
Purpose of the Study:
- To investigate the association between FST expression and the clinical characteristics and prognosis of breast cancer (BC), particularly TNBC.
- To elucidate the functional role of FST in TNBC cell proliferation, apoptosis, migration, and invasion.
Main Methods:
- Analysis of FST expression in 935 BC patient data from TCGA.
- Kaplan-Meier, COX, and ROC curve analyses to assess prognostic value.
- In vitro functional studies on TNBC cell lines (BT549, HS578T) involving FST knockdown.
- Bioinformatic analyses including volcanoplot, GO, KEGG, and PPI to explore FST's role in apoptotic pathways.
Main Results:
- Low FST expression significantly correlated with poor prognosis in BC and TNBC patients (HR=0.40, p=0.004).
- FST knockdown in TNBC cell lines promoted proliferation, migration, and invasion.
- FST inhibited apoptosis in mesenchymal TNBC cells by targeting BMP7.
Conclusions:
- Low FST expression is a marker for poor prognosis in TNBC.
- FST influences apoptosis differently in mesenchymal and mesenchymal stem-like TNBC cells but promotes proliferation and invasion in both subtypes.
- FST may serve as a subtype-heterogeneous biomarker for TNBC progression monitoring.
