Nuclear Factor κB Signaling and Its Related Non-coding RNAs in Cancer Therapy

Abstract

Nuclear factor κB (NF-κB) acts as a nuclear factor that is composed of five main subunits. It is a pluripotent and crucial dimer transcription factor that has a close relationship with many serious illnesses, especially its influences on cell proliferation, inflammation, and cancer initiation and progression. NF-κB acts as part of the signaling pathway and determines its effect on the expression of several other genes, such as epidermal growth factor receptor (EGFR), p53, signal transducer and activator of transcription 3 (STAT3), and non-coding RNA (ncRNA). Continuous activation of the NF-κB signaling pathway has been seen in many cancer types. While the NF-κB signaling pathway is tightly regulated in physiological settings, quite frequently it is constitutively activated in cancer, and the molecular biology mechanism underlying the deregulated activation of NF-κB signaling remains unclear. In this review, we discuss the regulatory role and possible clinical significance of ncRNA (microRNA [miRNA] and long non-coding RNA [lncRNA]) in NF-κB signaling in cancer, including in the conversion of inflammation to carcinogenesis. Non-coding RNA plays an essential and complex role in the NF-κB signaling pathway. NF-κB activation can also induce the ncRNA status. Targeting NF-κB signaling by ncRNA is becoming a promising strategy of drug development and cancer treatment.

Keywords: NF-κB; cancer therapy; nocoding RNA.