The Anticancer Effects of the Garlic Organosulfide Diallyl Trisulfide through the Attenuation of B[a]P-Induced Oxidative Stress, AhR Expression, and DNA Damage in Human Premalignant Breast Epithelial (MCF-10AT1) Cells.
Dominique T FergusonEquar TakaSyreeta L TilghmanTracy WombleBryan V RedmondShasline GedeonHernan Flores-RozasSarah L ReedKaram F A SolimanKonan J W KangaSelina F Darling-ReedPublished in: International journal of molecular sciences (2024)
Benzo[a]pyrene (B[a]P) is the most characterized polycyclic aromatic hydrocarbon associated with breast cancer. Our lab previously reported that the organosulfur compound (OSC), diallyl trisulfide (DATS), chemoprevention mechanism works through the induction of cell cycle arrest and a reduction in oxidative stress and DNA damage in normal breast epithelial cells. We hypothesize that DATS will inhibit B[a]P-induced cancer initiation in premalignant breast epithelial (MCF-10AT1) cells. In this study, we evaluated the ability of DATS to attenuate B[a]P-induced neoplastic transformation in MCF-10AT1 cells by measuring biological endpoints such as proliferation, clonogenicity, reactive oxygen species (ROS) formation, and 8-hydroxy-2-deoxyguanosine (8-OHdG) DNA damage levels, as well as DNA repair and antioxidant proteins. The results indicate that B[a]P induced proliferation, clonogenic formation, ROS formation, and 8-OHdG levels, as well as increasing AhR, ARNT/HIF-1β, and CYP1A1 protein expression compared with the control in MCF-10AT1 cells. B[a]P/DATS's co-treatment (CoTx) inhibited cell proliferation, clonogenic formation, ROS formation, AhR protein expression, and 8-OHdG levels compared with B[a]P alone and attenuated all the above-mentioned B[a]P-induced changes in protein expression, causing a chemopreventive effect. This study demonstrates, for the first time, that DATS prevents premalignant breast cells from undergoing B[a]P-induced neoplastic transformation, thus providing more evidence for its chemopreventive effects in breast cancer.
Keyphrases
- dna damage
- cell cycle arrest
- oxidative stress
- dna repair
- induced apoptosis
- cell death
- diabetic rats
- reactive oxygen species
- pi k akt
- high glucose
- signaling pathway
- cell proliferation
- endothelial cells
- squamous cell carcinoma
- breast cancer cells
- endoplasmic reticulum stress
- ischemia reperfusion injury
- poor prognosis
- drug induced
- long non coding rna
- nitric oxide
- combination therapy
- childhood cancer
- smoking cessation
- anti inflammatory
- replacement therapy