Regulation of Nuclear Factor-KappaB (NF-κB) signaling pathway by non-coding RNAs in cancer: Inhibiting or promoting carcinogenesis?

Mirzaei, S. and Zarrabi, A. and Hashemi, F. and Zabolian, A. and Saleki, H. and Ranjbar, A. and Seyed Saleh, S.H. and Bagherian, M. and Sharifzadeh, S.O. and Hushmandi, K. and Liskova, A. and Kubatka, P. and Makvandi, P. and Tergaonkar, V. and Kumar, A.P. and Ashrafizadeh, M. and Sethi, G. (2021) Regulation of Nuclear Factor-KappaB (NF-κB) signaling pathway by non-coding RNAs in cancer: Inhibiting or promoting carcinogenesis? Cancer Letters, 509. pp. 63-80.

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Abstract

The nuclear factor-kappaB (NF-κB) signaling pathway is considered as a potential therapeutic target in cancer therapy. It has been well established that transcription factor NF-κB is involved in regulating physiological and pathological events including inflammation, immune response and differentiation. Increasing evidences suggest that deregulated NF-κB signaling can enhance cancer cell proliferation, metastasis and also mediate radio-as well as chemo-resistance. On the contrary, non-coding RNAs (ncRNAs) have been found to modulate NF-κB signaling pathway under different settings. MicroRNAs (miRNAs) can dually inhibit/induce NF-κB signaling thereby affecting the growth and migration of cancer cells. Furthermore, the response of cancer cells to radiotherapy and chemotherapy may also be regulated by miRNAs. Regulation of NF-κB by miRNAs may be mediated via binding to 3/-UTR region. Interestingly, anti-tumor compounds can increase the expression of tumor-suppressor miRNAs in inhibiting NF-κB activation and the progression of cancers. Long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) can also effectively modulate NF-κB signaling thus affecting tumorigenesis. It is noteworthy that several studies have demonstrated that lncRNAs and circRNAs can affect miRNAs in targeting NF-κB activation. They can act as competing endogenous RNA (ceRNA) thereby reducing miRNA expression to induce NF-κB activation that can in turn promote cancer progression and malignancy. © 2021 Elsevier B.V.

Item Type: Article
Additional Information: cited By 5
Uncontrolled Keywords: antineoplastic agent; circular ribonucleic acid; competing endogenous RNA; curcumol; cyclooxygenase 2; doxorubicin; gemcitabine; heat shock protein 70; hydroxymethylglutaryl coenzyme A reductase kinase; immunoglobulin enhancer binding protein; long untranslated RNA; microRNA; mucin 1; paclitaxel; phosphatidylinositol 3 kinase; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase; protein bcl 2; RNA; schizandrin A; tanshinone IIA; tumor necrosis factor receptor associated factor 3; unclassified drug; untranslated RNA, 3' untranslated region; apoptosis; cancer chemotherapy; cancer inhibition; cancer radiotherapy; cancer risk; carcinogenesis; cell cycle arrest; cell differentiation; cell growth; cell maturation; cell proliferation; down regulation; drug targeting; enzyme activation; enzyme inhibition; epithelial mesenchymal transition; feedback system; gene expression regulation; gene function; human; immune response; malignant neoplasm; metastasis; NF kB signaling; nonhuman; protein expression; protein function; radiosensitivity; Review; treatment response; tumor promotion; upregulation
Subjects: QZ Pathology
Depositing User: eprints admin
Date Deposited: 01 Nov 2021 08:33
Last Modified: 01 Nov 2021 08:33
URI: http://eprints.iums.ac.ir/id/eprint/39161

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