Rho/ROCK and MAPK signaling pathways are involved in glioblastoma cell migration and proliferation.

Background: Glioblastoma multiforme (GBM) remains the most aggressive and frequently occurring brain neoplasm. Members of the Rho family of small GTP-binding proteins, including Rho, Rac, and Cdc42, have been shown to participate in cell growth differentiation and motility. The mitogen-activated protein kinase (MAPK) pathway, which includes extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), has been shown to regulate cell growth, differentiation and motility.

Gene expression profiling of metastatic brain cancer.

Gene expression profiling of metastatic brain tumors from primary lung adenocarcinoma, using a 17k-expression array, revealed that 1561 genes were consistently altered. Further functional classification placed the genes into seven categories: cell cycle and DNA damage repair, apoptosis, signal transduction molecules, transcription factors, invasion and metastasis, adhesion, and angiogenesis. Genes involved in apoptosis, such as caspase 2 (CASP2), transforming growth factor-beta inducible early gene (TIEG), and neuroprotective heat shock protein 70 (Hsp70) were underexpressed in metastatic brain tumors.

The antiproliferative effect of Quercetin in cancer cells is mediated via inhibition of the PI3K-Akt/PKB pathway.

Background: The tumor suppressor gene PTEN, mutated in 40-50% of patients with brain tumors, especially those with glioblastomas, maps to chromosome 10q23.3 and encodes a dual-specificity phosphatase. PTEN exerts its effects partly via inhibition of protein tyrosine kinase B (Akt/Protein Kinase B), which is involved in the phosphatidylinositol (PtdIns) 3-kinase (PI3K)-mediated cell-survival pathway.