Weiming Ouyang

TL;DR: Several recent studies have identified nuclear factor-κB as a key modulator in driving inflammation to cancers, and other proteins with extensive roles in inflammation and cancer, such as signal transducers and activators of transcription, Nrf2, and nuclear factor of activated T cells, are proposed to be promising targets for future studies.

TL;DR: It is found that exposure of Cl41 cells to arsenite was able to induce cell proliferation, activate PI-3K-->Akt/p70(S6k) signal pathway and increase cyclin D1 expression at both transcription and protein levels.

TL;DR: Exposure of human keratinocyte HaCat cells to arsenite resulted in the promotion of cell cycle progression, especially G(1) to S phase transition, and results show that arsenite-induced cell cycle is through IKKbeta/NF-kappaB/cyclin D1-dependent pathway.

TL;DR: Results show that p53 has a suppressive activity on the cell signaling pathways leading to activation of AP-1 and NF-kappaB in cell response to UV radiation, and PTEN is a well-known phosphatase involved in the regulation of phosphatidylinositol 3-kinase (PI-3K)/Akt signaling pathway, which may be a novel mechanism involved in anticancer activity of p53 protein.

TL;DR: It is demonstrated that PI-3K/Akt–mediated cyclin D1 expression is at least one key event implicated in the arsenite human skin carcinogenic effect.