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    NF-?B as a regulator of cancer metastasis and therapy response: A focus on epithelial-mesenchymal transition
    (Wiley, 2022) Mirzaei , Sepideh; Saghari, Sam; Bassiri, Farzaneh; Raesi, Rasoul; Zarrabi, Ali; Hushmandi, Kiavash; Sethi, Gautam; Tergaonkar, Vinay
    Metastasis of tumor cells is a complex challenge and significantly diminishes theoverall survival and prognosis of cancer patients. The epithelial?to?mesenchymaltransition (EMT) is a well?known mechanism responsible for the invasiveness oftumor cells. A number of molecular pathways can regulate the EMT mechanism incancer cells and nuclear factor?kappaB (NF??B) is one of them. The nucleartranslocation of NF??B p65 can induce the transcription of several genes involved inEMT induction. The present review describes NF??B and EMT interaction in cancercells and their association in cancer progression. Due to the oncogenic role NF??Bsignaling, its activation enhances metastasis of tumor cells via EMT induction. Thishas been confirmed in various cancers including brain, breast, lung and gastriccancers, among others. The ZEB1/2, transforming growth factor??, and Slug asinducers of EMT undergo upregulation by NF??B to promote metastasis of tumorcells. After EMT induction driven by NF??B, a significant decrease occurs inE?cadherin levels, while N?cadherin and vimentin levels undergo an increase. Thenoncoding RNAs can potentially also function as upstream mediators and modulateNF??B/EMT axis in cancers. Moreover, NF??B/EMT axis is involved in mediatingJ Cell Physiol. 2022;1–26.wileyonlinelibrary.com/journal/jcp© 2022 Wiley Periodicals LLC.|1Abbreviations:AREG, amphiregulin; circRNA, circular RNA; DLC?1, deleted in liver cancer?1; EMT, epithelial?to?mesenchymal transition; EMT?TFs, EMT?inducing transcription factors;FABP5, fatty acid?binding protein 5; GH, growth hormone; IGF1R, insulin like growth factor?1 receptor; IKK, I?B kinase; IL, interleukin; lncRNA, long noncoding RNA; MANF, mesencephalicastrocyte?derived neutrophic factor; miRNA, microRNA; NF??B, nuclear factor?kappaB; NIK, NF??B inducing kinase; SIRTs, sirtuins; SMC4, structural maintenance of chromosome 4;STAT3, signal transducer and activator of transcription 3; TGF??, transforming growth factor??; TLR?4, toll like growth factor?4; TNF, tumor necrosis factor. drug resistance in tumor cells. Thus, suppressing NF??B/EMT axis can also promotethe sensitivity of cancer cells to chemotherapeutic agents
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    Non-coding RNA-based regulation of inflammation
    (Elsevier Science, 2022) Ashrafizadeh, Milad; Zarrabi, Ali; Mostafavi, Ebrahim; Aref, Amir Reza; Sethi, Gautam; Wang, Lingzhi; Tergaonkar, Vinay
    nflammation is a multifactorial process and various biological mechanisms and pathways participate in its development. The presence of inflammation is involved in pathogenesis of different diseases such as diabetes mellitus, cardiovascular diseases and even, cancer. Non-coding RNAs (ncRNAs) comprise large part of tran- scribed genome and their critical function in physiological and pathological conditions has been confirmed. The present review focuses on miRNAs, lncRNAs and circRNAs as ncRNAs and their potential functions in inflam- mation regulation and resolution. Pro-inflammatory and anti-inflammatory factors are regulated by miRNAs via binding to 3’-UTR or indirectly via affecting other pathways such as SIRT1 and NF-?B. LncRNAs display a similar function and they can also affect miRNAs via sponging in regulating levels of cytokines. CircRNAs mainly affect miRNAs and reduce their expression in regulating cytokine levels. Notably, exosomal ncRNAs have shown ca- pacity in inflammation resolution. In addition to pre-clinical studies, clinical trials have examined role of ncRNAs in inflammation-mediated disease pathogenesis and cytokine regulation. The therapeutic targeting of ncRNAs using drugs and nucleic acids have been analyzed to reduce inflammation in disease therapy. Therefore, ncRNAs