Study type: In vitro · Status: Verified against declared source

Inhibiting the system xC−/glutathione axis selectively targets cancers with mutant-p53 accumulation

2017

Study scale: Mitochondrial-specific and generalized cellular ROS were detected using MitoSOX Red and CellROX Deep Red reagents respectively (ThermoFisher Scientific).

Abstract only: Open source record

Product or molecular entity relationships

Glutathione: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.

Plain-language verified summary

Question

Cells were reverse transfected with 40 nM p53, NRF2, SLC7A11 or non-targeting control siRNA pools (siGenome Smartpool, Dharmacon) using Lipofectamine RNAiMax solution (Life Technologies) according to the manufacturer's guidelines.

Methods

Mounting evidence indicates that cancer cells produce higher levels of ROS compared to normal cells, which in turn can activate mitogenic signalling and promote carcinogenesis7.

Scale or participants

Mitochondrial-specific and generalized cellular ROS were detected using MitoSOX Red and CellROX Deep Red reagents respectively (ThermoFisher Scientific).

Key findings

TP53, a critical tumour suppressor gene, is mutated in over half of all cancers resulting in mutant-p53 protein accumulation and poor patient survival.

Limitations and uncertainty

Mounting evidence indicates that cancer cells produce higher levels of ROS compared to normal cells, which in turn can activate mitogenic signalling and promote carcinogenesis7.

Verified against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.