Amphiphilic Photoluminescent Porous Silicon Nanoparticles as Effective Agents for Ultrasound-Amplified Cancer Therapy.

This study investigates the use of photoluminescent amphiphilic porous silicon nanoparticles (αϕ-pSiNPs) as effective ultrasound (US) amplifiers for cancer sonodynamic theranostics. αϕ-pSiNPs were synthesized via a novel top-down approach involving porous silicon (pSi) films electrochemical etching, borate oxidation, and hydrophobic coating with octadecylsilane (C18), resulting in milling into nanoparticles with hydrophilic exteriors and hydrophobic interiors. These properties promote gas trapping and cavitation nucleation, significantly lowering the US cavitation threshold and resulting in selective destruction of cancer cells in the presence of nanoparticles.

Ally or traitor: the dual role of p62 in caspase-2 regulation.

Caspase-2 is a unique and conserved cysteine protease that is involved in several cellular processes, including different forms of cell death, maintenance of genomic stability, and the response to reactive oxygen species. Despite advances in caspase-2 research in recent years, the mechanisms underlying its activation remain largely unclear. Although caspase-2 is activated in the PIDDosome complex, its processing could occur even in the absence of PIDD1 and/or RAIDD, suggesting the existence of an alternative platform for caspase-2 activation.

Cisplatin Resistance and Metabolism: Simplification of Complexity.

Cisplatin is one of the most well-known anti-cancer drugs and has demonstrated efficacy against numerous tumor types for many decades. However, a key challenge with cisplatin, as with any chemotherapeutic agent, is the development of resistance with a resultant loss of efficacy. This resistance is often associated with metabolic alterations that allow insensitive cells to divide and survive under treatment.

BH3-mimetics or DNA-damaging agents in combination with RG7388 overcome p53 mutation-induced resistance to MDM2 inhibition.

The development of drug resistance reduces the efficacy of cancer therapy. Tumor cells can acquire resistance to MDM2 inhibitors, which are currently under clinical evaluation. We generated RG7388-resistant neuroblastoma cells, which became more proliferative and metabolically active and were less sensitive to DNA-damaging agents in vitro and in vivo, compared with wild-type cells.

Cancer Drug Resistance: Targeting Proliferation or Programmed Cell Death.

The development of resistance to chemotherapy is one of the main problems for effective cancer treatment. Drug resistance may result from disturbances in two important physiological processes-cell proliferation and cell death. Importantly, both processes characterize alterations in cell metabolism, the level of which is often measured using MTT/MTS assays.