p53-mediated apoptosis is antagonized by growth factor stimulation. Here, we show that p53-dependent cell death induced by DNA damage was effectively prevented by mitogen activation. The levels of Bcl-2, Bcl-xL, and Bax were not altered by cisplatin treatment and mitogen rescue. Instead, the protection against p53-regulated apoptosis was mediated by at least three distinct signaling pathways. E...

The sphingolipid ceramide mediates various cellular processes in response to several extracellular stimuli. Some genotoxic stresses are able to induce p53-dependent ceramide accumulation leading to cell death. However, in other cases, in the absence of the tumor suppressor protein p53, apoptosis proceeds partly due to the activity of this "tumor suppressor lipid", ceramide. In the current revie...

The p53 tumor suppressor is the central component of a complex network of signaling pathways that protect organisms against the propagation of cells carrying oncogenic mutations. Here we report a previously unrecognized role of p53 in membrane phospholipids composition. By repressing the expression of stearoyl-CoA desaturase 1, SCD, the enzyme that converts saturated to mono-unsaturated fatty a...

Bladder cancer evolves via the accumulation of numerous genetic alterations, with loss of p53 and p16 function representing key events in the development of malignant disease. In addition, components of the epidermal growth factor receptor (EGFR) signaling pathway are frequently overexpressed, providing potential chemotherapeutic targets. We have previously described the generation of "paramali...

BACKGROUND Ovarian cancer is a cancerous growth arising from the ovary. OBJECTIVE This study was aimed to explore the molecular mechanism of the development and progression of the ovarian cancer. METHODS We first identified the differentially expressed genes (DEGs) between the ovarian cancer samples and the healthy controls by analyzing the GSE14407 affymetrix microarray data, and then the ...

CDCA7 is a copy number amplification gene that promotes tumorigenesis. However, the clinical relevance and potential mechanisms of in glioma are unclear. expression level data were obtained from Chinese Glioma Genome Atlas (CGGA) The Cancer (TCGA) databases, enriched genes related signaling pathways explored. Data on CDCA7-related nine marker ferroptosis retrieved protein–protein interaction (P...

Accumulating evidence shows that chronic inflammation can promote all stages of tumorigenesis, including DNA damage, limitless replication, apoptosis evasion, sustained angiogenesis, self-sufficiency in growth signaling, insensitivity to anti-growth signaling, and tissue invasion/metastasis. Chronic inflammation is triggered by environmental (extrinsic) factors (eg, infection, tobacco, asbestos...

The dynamic alterations in the cytoskeletal components actin and intermediate, etc. filaments are required for cell invasion migration. cytoskeleton is a highly structure that governed by delicate balance of filament formation disassembly. To controlling activities key epithelial mesenchymal transition (EMT) could be viable solution to metastasis. Bioinformatics technologies also allow research...

The dedifferentiation of the gastrointestinal stromal tumors (GISTs) has been reported in a small number cases, usually under pressure tyrosine kinase inhibitor (TKI) treatment. Herein, we described de novo dedifferentiated GIST with SDH deficiency 32-year-old Chinese woman. tumor was located on lesser curvature gastric antrum, measuring 4.1x9.1 cm 2 . Microscopically, composed distinct morphol...

In mice and humans the circadian rhythm of many biochemical reactions, physiology, and behavior is generated by a transcriptional-translation feedback loop (TTFL) made up of the so-called core clock genes/proteins. The circadian system interfaces with most signaling pathways including those involved in cell proliferation and inflammation. Cryptochrome (CRY) is a core clock protein that plays an...