Analyzing the Interaction Between HRAS, STAT3, and LRPPRC in the Mitochondria

Amelia Abell

Cancer is a leading cause of death worldwide, accounting for nearly one in six deaths, according to the World Health Organization (4). RAS genes (HRAS, NRAS, and KRAS in mammals) are the most frequently mutated oncogenes in human cancer and therefore, are considered one of the most important targets for anticancer therapy. (5). Acting as binary molecular switches, RAS genes alternate between a GDP (off) state and GTP (on) state. When in the GTP state, they transduce signals which regulate cell proliferation, differentiation, survival, and more (1). In the mutated oncogenic form of RAS, it remains solely in the GTP state, sending unwanted signals and causing unwanted processes (11,12). The dysregulation of these processes is considered a part of the hallmarks of cancer, which describe a set of functional capabilities acquired by normal human cells as they make their way to becoming malignant tumors (9). The various forms of RAS all have differing functions; HRAS has been found to be implicated most frequently in cervical, prostate, salivary gland, skin, digestive tract, and urinary tract cancers (12).