Evidence map›Paper›PMID 42477385›Full record

ArticleScientific reports2026

Enoxaparin induces apoptosis and autophagy, modulates inflammatory signaling, and reduces oxidative DNA damage in breast and liver cancer cells.

Sedat Carkit, Münevver Baran, Nazmiye Bitgen, Gozde Ozge Onder, Damla Gündüz, Arzu Yay

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Sedat CarkitDepartment of General Surgery, Erciyes University Faculty of Medicine, Kayseri, Turkey. sedatcarkit@erciyes.edu.tr.ORCID 0000-0001-7360-5121
Münevver BaranDepartment of Basic Sciences, Erciyes University Faculty of Pharmacy, Kayseri, Turkey.ORCID 0000-0003-0369-1022
Nazmiye BitgenDepartment of Medical Biology, Erciyes University Faculty of Medicine, Kayseri, Turkey.ORCID 0000-0002-6416-9230
Gozde Ozge OnderGenome and Stem Cell Center, Erciyes University, Kayseri, Turkey. gozdeozgekorkmaz@hotmail.com.ORCID 0000-0002-0515-9286
Damla GündüzDepartment of Histology and Embryology, Malatya Turgut Ozal University Faculty of Medicine, Malatya, Turkey.ORCID 0000-0003-4838-6574
Arzu YayGenome and Stem Cell Center, Erciyes University, Kayseri, Turkey.ORCID 0000-0002-0541-8372

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

ApoptosisAutophagyBreast NeoplasmsDNA DamageEnoxaparinLiver NeoplasmsOxidative StressCell Line, TumorCell SurvivalFemaleHEK293 CellsHep G2 CellsHumansInflammationMDA-MB-231 CellsNF-kappa BEnoxaparinNF-kappa BTumor Necrosis Factor-alpha8-OHdGApoptosisAutophagyInflammatory signalingOxidative DNA damage

Identifiers

PMID42477385
PMCPMC13554178

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.