Key result
Enoxaparin cuts oxidative DNA damage ~59% and reduces viability in breast and liver cancer cells.
Why the study?
Does enoxaparin reduce cell viability and induce apoptosis in breast and liver cancer cells?
Does enoxaparin reduce cell viability and induce apoptosis in breast and liver cancer cells?
Enoxaparin demonstrates direct anticancer effects in vitro by promoting apoptosis and autophagy, and reducing oxidative DNA damage in breast and liver cancer cell lines.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“A new study in Scientific Reports adds to the growing evidence that enoxaparin – long used simply to manage cancer-associated thrombosis – may have direct effects on tumour biology. The selectivity – hitting cancer cells while sparing normal cells – is what makes this interesting. It's in-vitro work, so it doesn't change clinical practice today, but it strengthens the rationale for exploring enoxaparin's role beyond thromboprophylaxis in oncology.”
Enoxaparin may modulate apoptosis and oxidative stress in cancer cells; leaves open any impact on clinical thrombosis management.
Cancer progression involves intricate interactions between inflammatory signaling, programmed cell death mechanisms, and oxidative stress. Although enoxaparin is widely used for managing cancer-associated thrombosis, its direct cellular effects on tumor biology remain insufficiently characterized. This study aimed to evaluate the impact of enoxaparin on apoptosis, autophagy, inflammatory mediators, and oxidative DNA damage in breast (MDA-MB-231) and liver (HepG2) cancer cell lines. MDA-MB-231, HepG2, and non-cancerous HEK-293 cells were treated with varying concentrations (5, 10, 20, 40, and 80 mg/mL) of enoxaparin for 24 and 48 h. Cell viability was assessed using the MTT assay, while apoptosis was quantified by TUNEL analysis. Immunofluorescence staining was employed to evaluate the expression of NF-κB, IL-6, TNF-α, LC3, and p62. Oxidative DNA damage was determined by measuring extracellular 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels using a competitive ELISA. Statistical analyses were conducted to compare the treated and control groups. Enoxaparin significantly reduced cell viability in MDA-MB-231 and HepG2 cells without inducing cytotoxicity in HEK-293 cells. Apoptosis was markedly increased in both cancer cell lines following treatment. Enoxaparin differentially modulated inflammatory signaling; NF-κB expression was significantly increased in MDA-MB-231 cells, accompanied by suppression of IL-6 and TNF-α, whereas no significant inflammatory changes were observed in HepG2 cells. Enoxaparin treatment was observed to increase LC3 and p62 expression in both MDA-MB-231 and HepG2 cells, triggering autophagy-related pathways. Moreover, enoxaparin significantly reduced extracellular 8-OHdG levels, suggesting a reduction in oxidative DNA damage. Enoxaparin exhibits multifaceted anticancer effects by promoting apoptosis and autophagy, selectively modulating inflammatory pathways, and reducing oxidative DNA damage in breast and liver cancer cells.
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Çarkıt et al. (2026) studied Breast and liver cancer. Enoxaparin vs. Untreated control was evaluated on Extracellular 8-OHdG levels in MDA-MB-231 cells (p=<0.0001). Enoxaparin significantly reduced cell viability, increased apoptosis and autophagy, and reduced oxidative DNA damage in MDA-MB-231 breast and HepG2 liver cancer cells.
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