p62 | Ricerc@Sapienza

Kaposi Sarcoma Herpes Virus (KSHV) infection inhibits macrophage formation and survival by counteracting Macrophage Colony-Stimulating Factor (M-CSF)-induced increase of Reactive Oxygen Species (ROS), c-Jun N-terminal kinase (JNK) phosphorylation and

Kaposi Sarcoma Herpes Virus (KSHV) is an oncovirus belonging to the human gammaherpesvirus family, able to infect several immune cell types including B cells, dendritic cells (DCs) and monocytes. In this study, we found that KSHV infection of monocytes counteracted the Reactive Oxygen Species (ROS) increase induced by Macrophage Colony-Stimulating Factor (M-CSF), prevented c-Jun N-terminal kinase (JNK) and B-cell lymphoma-2 (Bcl-2) phosphorylation and inhibited autophagy, leading to an impairment of cell survival and differentiation into macrophages.

Mutant p53, stabilized by its interplay with HSP90, activates a positive feed-back loop between NRF2 and p62 that induces chemio-resistance to Apigenin in pancreatic cancer cells

Pancreatic cancer is one of the most aggressive cancers whose prognosis is worsened by the poor response to the current chemotherapies. In this study, we investigated the cytotoxic effect of Apigenin, against two pancreatic cell lines, namely Panc1 and PaCa44, harboring different p53 mutations. Apigenin is a flavonoid widely distributed in nature that displays anti-inflammatory and anticancer properties against a variety of cancers. Here we observed that Apigenin exerted a stronger cytotoxic effect against Panc1 cell line in comparison to PaCa44.