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Review
. 2022 Nov;86(Pt 2):697-708.
doi: 10.1016/j.semcancer.2022.03.019. Epub 2022 Mar 26.

Epigenetic regulation of CXCR4 signaling in cancer pathogenesis and progression

Reem Khaled M E Alsayed  1 , Abdul Q Khan  1 , Fareed Ahmad  2 , Abdul Wahid Ansari  2 , Majid Ali Alam  2 , Jorg Buddenkotte  2 , Martin Steinhoff  3 , Shahab Uddin  4 , Aamir Ahmad  5
Affiliations
Free article
Review

Epigenetic regulation of CXCR4 signaling in cancer pathogenesis and progression

Reem Khaled M E Alsayed et al. Semin Cancer Biol. 2022 Nov.
Free article

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.

Keywords: CXCR; Epigenetic; Methylation/acetylation; Non-coding RNA; SDF-1/CXCL12.

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Conflict of interest statement

Conflict of Interest Statement None of the authors have any conflict of interest to report.

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