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Nuclear Factor κB Signaling and Its Related Non-coding RNAs in Cancer Therapy
Xiaomin Liu1, Yang Shao2, Jinbao Zhou2
1School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China; Lab for Noncoding RNA & Cancer, School of Life Sciences, Shanghai University, Shanghai 200444, China.
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.
Insights
Non-coding RNAs (ncRNAs) regulate the Nuclear factor κB (NF-κB) signaling pathway, which is crucial in cancer development and progression. Targeting ncRNAs offers a promising strategy for novel cancer drug development and treatment.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- Nuclear factor κB (NF-κB) is a key transcription factor involved in cell proliferation, inflammation, and cancer.
- Dysregulated NF-κB signaling is implicated in numerous cancer types, often leading to constitutive activation.
- NF-κB influences the expression of genes like EGFR, p53, STAT3, and non-coding RNAs (ncRNAs).
Purpose of the Study:
- To review the regulatory role of ncRNAs (miRNAs and lncRNAs) in NF-κB signaling within the context of cancer.
- To discuss the clinical significance of ncRNA-mediated regulation of NF-κB in carcinogenesis.
- To explore the complex interplay between ncRNAs and NF-κB signaling.
Main Methods:
- Literature review focusing on ncRNA regulation of NF-κB signaling in cancer.
- Analysis of molecular mechanisms linking ncRNAs, NF-κB, and cancer progression.
- Discussion of potential therapeutic strategies targeting this pathway.
Main Results:
- Non-coding RNAs play a significant and intricate role in modulating NF-κB signaling.
- NF-κB activation can, in turn, influence the expression or status of ncRNAs.
- The interaction between ncRNAs and NF-κB is crucial in the inflammation-to-carcinogenesis transition.
Conclusions:
- Targeting NF-κB signaling through ncRNAs presents a promising avenue for cancer drug development.
- Modulating ncRNA activity offers potential therapeutic strategies for cancer treatment.
- Understanding the ncRNA-NF-κB axis is vital for advancing cancer therapy.
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