Document Type : Original Article
Authors
1
Department of Biology, Faculty of Mathematics and Natural Sciences, Universitas Indonesia, Depok Campus, Depok, 16424, Indonesia.
2
Department of Medical Chemistry, Faculty of Medicine, Universitas Indonesia, Jakarta, 10440, Indonesia. Depok Campus, Depok, 16424, Indonesia.
3
Cellular and Molecular Mechanisms in Biological System Research Group, Department of Biology, Faculty of Mathematics and Natural Sciences, Universitas Indonesia, Depok Campus, Depok, 16424, Indonesia.
4
Institute for Advanced Sustainable Materials Research and Technology (INA-SMART), Faculty of Mathematics and Natural Science, Universitas Indonesia, Depok 16424, Indonesia.
5
Cellular and Molecular Mechanisms in Biological System Research Group, Department of Biology, Faculty of Mathematics and Natural Sciences, Universitas Indonesia, Depok Campus, Depok, 16424, Indonesia
Abstract
Triple-negative breast cancer (TNBC) is an aggressive subtype defined by the lack of
estrogen receptors (ER), progesterone receptors (PR), and HER2 expression, resulting
in limited therapeutic options. Given this challenge, this study explores caffeine, a
widely consumed stimulant, as a potential anticancer agent, particularly for TNBC.
Although caffeine has demonstrated stimulatory and inhibitory effects on telomerase
in other cancer types, its influence on telomerase activity in TNBC remains
uncharacterized. This study investigates the impact of caffeine concentrations (10, 15,
and 20 mM) on cell viability, proliferation, apoptosis, ultrastructure, and the
expression of apoptosis-related genes (BAX, BCL2, CASP8) and telomerase activity
(hTERT) in MDA-MB-231 cells. Our findings showed that caffeine significantly
reduces cell viability and induces early apoptosis with a dose-dependent effect.
Morphological changes consistent with early apoptosis were observed, and an
increased BAX/BCL2 ratio indicated the activation of the intrinsic apoptosis pathway.
Additionally, caffeine exhibited upregulation of hTERT mRNA expression, which may
reflect a compensatory response to cellular stress induced by caffeine. These results
underscore the multifaceted effects of caffeine on TNBC cells, highlighting its
potential not only as an apoptosis inducer but also as a modulator of telomerase
activity. Given its accessibility, low toxicity, and established safety profile, caffeine
presents an exciting avenue for further research as a complementary or standalone
therapeutic strategy for TNBC.
Keywords