Targeting Oxidative Stress in Cancer

Mandal, Paramita; Goswami, Anindita; Adhikari, Sarmistha; Sarkar, Subham

doi:10.1007/978-981-15-9411-3_19

Cited by 1 publication

(1 citation statement)

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“…Treatment with natural compounds, such as RESV and anticancer drugs causes an imbalance in the reactive oxygen levels, which leads to apoptosis via P53 and mitochondrial cytochrome release [46]. This imbalance between the production and elimination of ROS, and the biological system's capacity to quickly detoxify the reactive intermediates or to repair the damage that results is known as oxidative stress [47]. ROS production can cause oxidative stress with severe DNA damage to the cells via the initiation, promotion, and progression mechanisms [48].…”

Section: Discussionmentioning

confidence: 99%

Enhancement of reactive oxygen species production in triple negative breast cancer cells treated with electric pulses and resveratrol

Giri

Camarillo

Sundararajan

2023

Exploration of Targeted Anti-Tumor Therapy

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Aim: Triple negative breast cancer (TNBC) is difficult to treat since it lacks all the three most commonly targeted hormone receptors. Patients afflicted with TNBC are treated with platinum core chemotherapeutics, such as cisplatin. Despite the initial effective anticancer effects of cisplatin, TNBC attenuates its effect and develops resistance eventually, which results in tumor reoccurrence. Hence, there is a critical demand for effective, alternative, and natural ways to treat TNBC. Towards this, a promising technique for inhibiting TNBC cell proliferation involves promoting the production of reactive oxygen species (ROS), which triggers pro-apoptotic caspases 9 and 3. Resveratrol (RESV), an active bio compound found in naturally available fruits, such as grapes, is utilized in this research for that. In addition, electrochemotherapy (ECT), which involves the application of electrical pulses (EP), was utilized to enhance the uptake of RESV. Methods: MDA-MB-231, human TNBC cells were treated with/out RESV, and eight 600–1,000 V/cm, 100 μs pulses at 1 Hz. The cells were characterized by using various assays, including viability assay, and ROS assay. Results: A TNBC cell viability of as low as 20% was obtained at 24 h (it was 13% at 60 h), demonstrating the potential of this novel treatment. ROS production was the highest in the combination of EP at 1,000 V/cm along with RESV at 100 μmol/L. Conclusions: Results indicate that RESV has the potential as an anti-TNBC agent and that EP + RESV can significantly enhance the cell death to reduce MDA-MB-231 cell viability by increasing ROS production and triggering apoptosis.

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Section: Discussionmentioning

confidence: 99%