ELF3 plays an important role in defining TRAIL sensitivity in breast cancer by modulating the expression of decoy receptor 2 (DCR2).

Background: TRAIL protein on binding to its cognate death receptors (DR) can induce apoptosis specifically in breast tumor cells sparing normal cells. However, TRAIL also binds to decoy receptors (DCR) thereby inhibiting the apoptotic pathways thus causing TRAIL resistance. Also, one of the barriers due to which TRAIL-based therapy could not become FDA-approved might be because of resistance to therapy.

Anion-directed structural tuning of two azomethine-derived Zn complexes with optoelectronic recognition of Cu in aqueous medium with anti-cancer activities: from micromolar to femtomolar sensitivity with DFT revelation.

Herein, two novel mononuclear transition metal Zn complexes [Zn(HL)(N)(OAc)] (NS-1) & [Zn(HL)(ClO)] (NS-2) have been synthesised using a tridentate clickable Schiff base ligand, HL (2-methyl-2-((pyridin-2-ylmethyl)amino)propan-1-ol), and the polyatomic monoanions N and ClO for NS-1 and NS-2 respectively. Interestingly, NS-1 and NS-2 have been explored for the detection of Cu with an LOD of 48.6 fM (response time ∼6 s) and 2.

CDH1 overexpression sensitizes TRAIL resistant breast cancer cells towards rhTRAIL induced apoptosis.

Purpose: Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is well known for its unique ability to induce apoptosis in cancer cells but not normal cells. However, a subpopulation of cancer cells exist that does not respond to toxic doses of TRAIL. In this study, we aimed to identify key factors regulating TRAIL resistance in breast cancer.

Reactive oxygen species-dependent upregulation of death receptor, tumor necrosis factor receptor 1, is responsible for theophylline-mediated cytotoxicity in MDA-MB-231 breast cancer cells.

Theophylline, a methylxanthine drug, has been used as a therapy for respiratory diseases. Recently, it has also been shown to have a potential in treating different cancers. Also, it has shown promising results in clinical trials for AML in combination therapy.

Mechanism of melatonin protection against copper-ascorbate-induced oxidative damage in vitro through isothermal titration calorimetry.

Aims: Involvement of oxidative stress in cardiovascular diseases is well established. Melatonin's role as an antioxidant and free radical scavenger via its receptor dependent and receptor independent pathways is well known. The aim of this study is to identify and elaborate upon a third mechanism by which melatonin is able to abrogate oxidative stress.