ArticleTranslational cancer research2026
EGCG promotes apoptosis in BT-549 triple-negative breast cancer cells by targeting STAT3.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Triple-negative breast cancer (TNBC), defined by the lack of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression, is an aggressive subtype of breast cancer (BC) with limited therapeutic options. Signal transducer and activator of transcription 3 (STAT3) plays a critical oncogenic role in TNBC by promoting tumor progression and conferring resistance to apoptosis. (-)-epigallocatechin-3-gallate (EGCG), a bioactive green tea polyphenol, has been reported to inhibit STAT3 signaling and exert anti-cancer effects. However, its mechanistic effect on STAT3-mediated pathways in TNBC has yet to be fully elucidated. This study aims to investigate the effects of EGCG on TNBC cell proliferation, migration, and apoptosis, and to elucidate the underlying mechanisms involving STAT3-associated signaling and hydrogen sulfide-related pathways. Methods: BT-549 TNBC cells were treated with EGCG to assess its effects on cell viability, migration, and apoptosis. STAT3 expression was assessed at both the transcript and protein levels. Apoptotic regulatory proteins, including Bax, Bcl-2, caspase-3, and caspase-8, were quantified to examine pathway involvement. Molecular docking and molecular dynamics simulations were conducted to evaluate the interaction between EGCG and STAT3, and to explore the potential inhibition of the JAK/STAT3/ERK signaling cascade. Results: EGCG significantly reduced the viability, impaired the migratory capacity, and significantly enhanced the apoptosis of BT-549 cells. The treatment significantly downregulated STAT3 at both the messenger RNA (mRNA) and protein levels. EGCG further modulated apoptotic regulators by increasing the Bax/Bcl-2 ratio and promoting the activation of caspase-3 and caspase-8. Computational analyses revealed a stable binding interaction between EGCG and STAT3, which supporting the inhibitory effect on the JAK/STAT3/ERK signaling axis. Conclusions: EGCG effectively suppresses STAT3-driven oncogenic signaling in TNBC by inhibiting cell proliferation, reducing migration, and inducing apoptosis through the modulation of key apoptotic pathways. Thus, EGCG could be a promising therapeutic candidate for targeting STAT3-mediated mechanisms in TNBC. Further research should be conducted to examine the clinical application of EGCG.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.