Effects of Mutant KRASG12C on Chemotherapeutic Resistance in Lung Cancer

Abstract

The oncogene KRAS, a small GTPase, is a known cancer driver gene in human lung tumors. Mutations result in contitutive activation and excessive cell growth, leading to disease progression. Using lipsomal transfection, KRASG12C was introduced into human lung cancer cell lines. Western blot was used to confirm overexpression of exogenous KRASG12C from endogenous KRAS within the cell lines. Once transient expression was established, cell lines were challenged with Paclitaxel, a common chemotherapeutic drug, and cell viability was assessed. Survival of parental cell lines was compared to those overexpressing KRASG12C to determine the role of this mutation in paclitaxel sensitivity.