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  1. Article ; Online: Epigenetic programing of cancer stemness by transcription factors-non-coding RNAs interactions.

    Alsayed, Reem Khaled M E / Sheikhan, Khalid Sultan A M / Alam, Majid Ali / Buddenkotte, Jorg / Steinhoff, Martin / Uddin, Shahab / Ahmad, Aamir

    Seminars in cancer biology

    2023  Volume 92, Page(s) 74–83

    Abstract: Cancer 'stemness' is fundamental to cancer existence. It defines the ability of cancer cells to indefinitely perpetuate as well as differentiate. Cancer stem cell populations within a growing tumor also help evade the inhibitory effects of chemo- as well ...

    Abstract Cancer 'stemness' is fundamental to cancer existence. It defines the ability of cancer cells to indefinitely perpetuate as well as differentiate. Cancer stem cell populations within a growing tumor also help evade the inhibitory effects of chemo- as well as radiation-therapies, in addition to playing an important role in cancer metastases. NF-κB and STAT-3 are representative transcription factors (TFs) that have long been associated with cancer stemness, thus presenting as attractive targets for cancer therapy. The growing interest in non-coding RNAs (ncRNAs) in the recent years has provided further insight into the mechanisms by which TFs influence cancer stem cell characteristics. There is evidence for a direct regulation of TFs by ncRNAs, such as, microRNAs (miRNAs), long non-coding RNAs (lncRNAs) as well as circular RNAs (circRNAs), and vice versa. Additionally, the TF-ncRNAs regulations are often indirect, involving ncRNA-target genes or the sponging of other ncRNA species by individual ncRNAs. The information is rapidly evolving and this review provides a comprehensive review of TF-ncRNAs interactions with implications on cancer stemness and in response to therapies. Such knowledge will help uncover the many levels of tight regulations that control cancer stemness, providing novel opportunities and targets for therapy in the process.
    MeSH term(s) Humans ; Transcription Factors/genetics ; RNA, Untranslated/genetics ; MicroRNAs/genetics ; Neoplasms/genetics ; Epigenesis, Genetic
    Chemical Substances Transcription Factors ; RNA, Untranslated ; MicroRNAs
    Language English
    Publishing date 2023-04-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2023.04.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Epigenetic control of inflammation in Atopic Dermatitis.

    Akhtar, Sabah / Alsayed, Reem Khaled M E / Ahmad, Fareed / AlHammadi, Ayda / Al-Khawaga, Sara / AlHarami, Sara Mohamed A M / Alam, Majid Ali / Al Naama, Khalifa Abdulla H N / Buddenkotte, Joerg / Uddin, Shahab / Steinhoff, Martin / Ahmad, Aamir

    Seminars in cell & developmental biology

    2023  Volume 154, Issue Pt C, Page(s) 199–207

    Abstract: Atopic dermatitis (AD), also known as atopic eczema, is a common but also complex chronic, itchy skin condition with underlying inflammation of the skin. This skin ailment is prevalent worldwide and affects people of all ages, particularly children below ...

    Abstract Atopic dermatitis (AD), also known as atopic eczema, is a common but also complex chronic, itchy skin condition with underlying inflammation of the skin. This skin ailment is prevalent worldwide and affects people of all ages, particularly children below five years of age. The itching and resulting rashes in AD patients are often the result of inflammatory signals, thus necessitating a closer look at the inflammation-regulating mechanisms for putative relief, care and therapy. Several chemical- as well as genetically-induced animal models have established the importance of targeting pro-inflammatory AD microenvironment. Epigenetic mechanisms are gaining attention towards a better understanding of the onset as well as the progression of inflammation. Several physiological processes with implications in pathophysiology of AD, such as, barrier dysfunction either due to reduced filaggrin / human β-defensins or altered microbiome, reprograming of Fc receptors with resulting overexpression of high affinity IgE receptors, elevated eosinophil numbers or the elevated IL-22 production by CD4 + T cells have underlying epigenetic mechanisms that include differential promoter methylation and/or regulation by non-coding RNAs. Reversing these epigenetic changes has been verified to reduce inflammatory burden through altered secretion of cytokines IL-6, IL-4, IL-13, IL-17, IL-22 etc, with benefit against AD progression in experimental models. A thorough understanding of epigenetic remodeling of inflammation in AD has the potential of opening avenues for novel diagnostic, prognostic and therapeutic options.
    Language English
    Publishing date 2023-04-27
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2023.04.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Epigenetic regulation of CXCR4 signaling in cancer pathogenesis and progression.

    Alsayed, Reem Khaled M E / Khan, Abdul Q / Ahmad, Fareed / Ansari, Abdul Wahid / Alam, Majid Ali / Buddenkotte, Jorg / Steinhoff, Martin / Uddin, Shahab / Ahmad, Aamir

    Seminars in cancer biology

    2022  Volume 86, Issue Pt 2, Page(s) 697–708

    Abstract: Signaling involving chemokine receptor CXCR4 and its ligand SDF-1/CXL12 has been investigated for many years for its possible role in cancer progression and pathogenesis. Evidence emerging from clinical studies in recent years has further established ... ...

    Abstract Signaling involving chemokine receptor CXCR4 and its ligand SDF-1/CXL12 has been investigated for many years for its possible role in cancer progression and pathogenesis. Evidence emerging from clinical studies in recent years has further established diagnostic as well as prognostic importance of CXCR4 signaling. CXCR4 and SDF-1 are routinely reported to be elevated in tumors, distant metastases, which correlates with poor survival of patients. These findings have kindled interest in the mechanisms that regulate CXCR4/SDF-1 expression. Of note, there is a particular interest in the epigenetic regulation of CXCR4 signaling that may be responsible for upregulated CXCR4 in primary as well as metastatic cancers. This review first lists the clinical evidence supporting CXCR4 signaling as putative cancer diagnostic and/or prognostic biomarker, followed by a discussion on reported epigenetic mechanisms that affect CXCR4 expression. These mechanisms include regulation by non-coding RNAs, such as, microRNAs, long non-coding RNAs and circular RNAs. Additionally, we also discuss the regulation of CXCR4 expression through methylation and acetylation. Better understanding and appreciation of epigenetic regulation of CXCR4 signaling can invariably lead to identification of novel therapeutic targets as well as therapies to regulate this oncogenic signaling.
    MeSH term(s) Humans ; Epigenesis, Genetic ; Chemokine CXCL12/genetics ; Receptors, CXCR4/genetics ; Neoplasms/genetics ; Signal Transduction/genetics ; Prognosis ; MicroRNAs/genetics
    Chemical Substances Chemokine CXCL12 ; Receptors, CXCR4 ; MicroRNAs ; CXCR4 protein, human
    Language English
    Publishing date 2022-03-26
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2022.03.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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