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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-Mediated N6-Methyladenosine (m6A) deposition: A pivotal regulator of cancer, impacting key signaling pathways in carcinogenesis and therapy response
    (Keai Publishing Ltd, 2024) Hashemi, Mehrdad; Daneii, Pouria; Zandieh, Mohammad Arad; Raesi, Rasoul; Zahmatkesh, Neda; Bayat, Mehrsa; Abuelrub, Anwar
    The emergence of RNA modifications has recently been considered as critical post-transcriptional regulations which governed gene expression. N6-methyladenosine (m6A) modification is the most abundant type of RNA modification which is mediated by three distinct classes of proteins called m6A writers, readers, and erasers. Accumulating evidence has been made in understanding the role of m6A modification of non-coding RNAs (ncRNAs) in cancer. Importantly, aberrant expression of ncRNAs and m6A regulators has been elucidated in various cancers. As the key role of ncRNAs in regulation of cancer hallmarks is well accepted now, it could be accepted that m6A modification of ncRNAs could affect cancer progression. The present review intended to discuss the latest knowledge and importance of m6A epigenetic regulation of ncRNAs including mircoRNAs, long non-coding RNAs, and circular RNAs, and their interaction in the context of cancer. Moreover, the current insight into the underlying mechanisms of therapy resistance and also immune response and escape mediated by m6A regulators and ncRNAs are discussed.
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    Targeting AMPK signaling in ischemic/reperfusion injury: From molecular mechanism to pharmacological interventions
    (2022) Paskeh, Mahshid Deldar Abad; Asadi, Ava; Mirzaei, Sepideh; Hashemi, Mehrdad; Entezari, Maliheh; Raesi, Rasoul; Hushmandi, Kiavash; Zarrabi, Ali; Ertas, Yavuz Nuri; Aref, Amir Reza; Samarghandian, Saeed; Reiter, Russel J; Ren, Jun
    Ischemia is a pathological process in which blood supply to a particular organ is temporarily interrupted resulting in disturbed biological function and homeostasis of local tissues. Following ischemia, reperfusion and reoxygenation may occur which further worsens oxidative stress-mediated damage in cells and tissues. The combined processes are referred to as ischemia/reperfusion (I/R) injury. Immediate management and treatment of I/R is of utmost importance for preventing irreversible and extensive cellular damage. Apoptosis, inflammation and oxidative stress are the most validated pathologies associated with I/R. AMP-activated protein kinase (AMPK) modulates energy metabolism in cells and its activation occurs in response to elevated AMP and ADP levels. Aberrant levels of AMPK are noted in various pathological settings such as diabetes mellitus, cancer and neurological diseases. This review emphasizes AMPK signaling, its related molecular pathways and therapeutic utility during I/R. Activation of AMPK through phosphorylation prevents apoptosis and reduces oxidative stress and inflammation upon I/R. Inducing AMPK signaling normalizes mitochondrial function to inhibit cell death. Autophagy as a cytoprotective mechanism undergoes activation by AMPK/mTOR and AMPK/ULK1 pathways. AMPK reinforces the antioxidant defense capacity via Nrf2 signaling to counteract oxidative stress in I/R. Protective compounds including phytochemicals activate AMPK to alleviate I/R injury.
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    Targeting Nrf2 in ischemia-reperfusion alleviation: From signaling networks to therapeutic targeting
    (Elsevier Inc., 2022) Sadrkhanloo, Mehrdokht; Entezari, Maliheh; Orouei, Sima; Zabolian, Amirhossein; Mirzaie, Amirreza; Maghsoudloo, Amin; Raesi, Rasoul; Asadi, Neda; Hashemi, Mehrdad; Zarrabi, Ali; Khan, Haroon; Mirzaei, Sepideh; Samarghandian, Saeed
    The nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of redox balance and it responds to various cell stresses that oxidative stress is the most well-known one. The Nrf2 should undergo nuclear translocation to exert its protective impacts and decrease ROS production. On the other hand, ischemic/reperfusion (I/R) injury is a pathological event resulting from low blood flow to an organ and followed by reperfusion. The I/R induces cell injury and organ dysfunction. The present review focuses on Nrf2 function in alleviation of I/R injury. Stimulating of Nrf2 signaling ameliorates I/R injury in various organs including lung, liver, brain, testis and heart. The Nrf2 enhances activity of antioxidant enzymes to reduce ROS production and prevent oxidative stress-mediated cell death. Besides, Nrf2 reduces inflammation via decreasing levels of pro-inflammatory factors including IL-6, IL-1? and TNF-?. Nrf2 signaling is beneficial in preventing apoptosis and increasing cell viability. Nrf2 induces autophagy to prevent apoptosis during I/R injury. Furthermore, it can interact with other molecular pathways including PI3K/Akt, NF-?B, miRNAs, lncRNAs and GSK-3? among others, to ameliorate I/R injury. The therapeutic agents, most of them are phytochemicals such as resveratrol, berberine and curcumin, induce Nrf2 signaling in I/R injury alleviation. © 2022