Retinoic acid receptor (RAR) signaling plays an important role in embryonic development and homeostasis of many tissues. At the cellular level, activation of RAR signaling often induces cell cycle arrest, differentiation, and apoptosis in many types of cells. Consequently, loss of normal RAR function in the presence of physiological levels of retinoic acid (RA) is often observed in cancers, and pharmacological reactivation of RAR signaling has been considered a promising strategy for cancer therapy and prevention. One of important mechanisms that regulate RAR activity in cancer cells is cross-talk with growth factor signaling, where activation of extracellular signal-regulated kinase (ERK) plays a major role in suppressing RAR transcriptional activity downstream of growth factor receptors. Conversely, strong activation of RAR can induce suppression of ERK activity by inducing expression of a phosphatase specific for ERK to exert tumor-suppressive activity in colorectal cancer. Here, we describe the basic methods to analyze interactions between RAR and ERK signaling in colorectal cancer cells.
Keywords: Colorectal cancer; ERK MAP kinase; Growth factor signaling; Retinoic acid receptor (RAR); Retinoid.