Role and Regulation of Transcriptional Factors in Gastric Cancer
Gastric cancer is the second major cancer diagnosed worldwide. Cytokines, chemokines, metalloproteinases, prostaglandins, and reactive oxygen nitrogen species induce, amplify, and sustain inflammation (in the lining of the stomach) in the host. Signalling pathways like β-catenin, NF-κB, etc. bring about changes in the genetic material leading to diversification of genetic material. Genetic diversification in oncogenes and tumour suppressor genes leads to gastric cancer. Transcriptional factors’ role in apoptosis, cell cycle, cell proliferation, and metastasis (adhesion, invasion, migration, angiogenesis) is well known and established. The role and regulation of transcriptional factors in relation to gastric cancer was reviewed.
Abstract Apoptotic cells are removed from tissues by uptake mechanisms that depend on the GTPase Rac (CED-10 in C. elegans ), which is activated by DOCK180/CED-5 in a trimolecular complex with ELMO/CED-12 and CrkII/CED-2. A study now identifies upstream components of this pathway in both worms and mammalian cells involving yet another GTPase, RhoG/MIG-2, and its activator TRIO/UNC-73.