Down-regulated FST expression is involved in the poor prognosis of triple-negative breast cancer.
Level 3 - non-randomized controlled study
Retrospective observational cohort analysis of public genomic data (TCGA) combined with in vitro experiments
PubMed 34001106 · doi:10.1186/s12935-021-01977-x
What was done
Investigators extracted clinical and genomic data from 935 breast cancer patients in The Cancer Genome Atlas (TCGA) to assess the relationship between follistatin (FST) expression and prognosis using Kaplan-Meier, univariate/multivariate Cox regression, and ROC curve analyses. Functional in vitro assays were performed on TNBC cell lines (BT549 and HS578T) to evaluate proliferation, apoptosis, migration, and invasion following FST knockdown, complemented by bioinformatic pathway and protein-protein interaction analyses.
What was found
Low FST expression was significantly associated with poor prognosis in univariate analysis (HR = 0.47, 95% CI: 0.27 to 0.82, p = 0.008) and multivariate analysis (HR = 0.40, 95% CI: 0.21 to 0.75, p = 0.004). Functional knockdown of FST promoted proliferation, migration, and invasion in BT549 and HS578T cell lines, while FST inhibited mesenchymal cell apoptosis by targeting BMP7.
Why it matters
These findings suggest that down-regulated FST may serve as a subtype-heterogeneous prognostic biomarker and functional driver of tumor aggressiveness in triple-negative breast cancer.
Limits
The clinical correlation is based entirely on retrospective data from a single database (TCGA) without an independent validation cohort. The exact sample size for the TNBC subgroup among the 935 patients is not stated in the abstract, and mechanistic findings are restricted to in vitro cell models without in vivo confirmation.
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