Posttranscriptional control of the chemokine receptor CXCR4 expression in cancer cells

Al-Souhibani, Norah; Alghamdi, Metib; Al-Ahmadi, Wijdan; Khabar, Khalid S.A.

doi:10.1093/carcin/bgu080

Cited by 35 publications

(39 citation statements)

References 47 publications

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“…Cancer cells characteristically express CD44, and there is increasing evidence that HCELL serves as their major selectin ligand. This finding clarifies the ability of solid tumors to infiltrate bone marrow that is both HCELL and CXCR4 dependent [137][138][139] . Variations in CD44 are reported as cell surface markers for breast cancer stem cells.…”

Section: Cd44supporting

confidence: 62%

The role of adhesion molecules in acute myeloid leukemia and (hemato)oncology: A systematic review

Kupsa¹,

Horáček²,

Jebavý³

2015

BIOMED PAP

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Background. The treatment of malignancies like acute myeloid leukemia (AML) is often complicated by the heterogeneity of the disease and the mechanisms of the disease progression. This heterogeneity is often not reflected in standard treatment approaches which provide predictable outcomes in the majority of patients but fail in individual cases even with high-dose multi-agent chemotherapy regimens and allogeneic stem cell transplantation. Further, the unselective effect of chemotherapy causes high treatment-related toxicity and accelerates the risk of infection during prolonged pancytopenia, preventing further dose escalation. Despite rapid progress in therapeutic strategies, the fatality of high-grade malignancies remains enormous. Objectives. Adhesive interactions trigger signal transduction pathway activation and this prevents the apoptosis of both normal and malignant cells. A correlation between expression of defined adhesion molecules and patient outcome has been found for several malignant diseases including AML. We aim to describe how disruption of these signalling pathways can overcome the high resistance to treatment and increase the selectivity of targeting malignant cells. This could effectively reduce the overall treatment-related toxicity and improve the general outcome. Conclusions. Adhesion molecules facilitate growth of malignant diseases. This review provides a deeper insight into these processes. Modulation of adhesion molecules-mediated interactions is an innovative and feasible approach in treatment of AML and many other malignancies. Due to expected low toxicity it is an acceptable addition to standard chemotherapeutical regimens for all age groups of patients. This approach could improve the overall treatment outcome in the future.

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Section: Cd44supporting

confidence: 62%

The role of adhesion molecules in acute myeloid leukemia and (hemato)oncology: A systematic review

Kupsa¹,

Horáček²,

Jebavý³

2015

BIOMED PAP

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“…Cotransfection with RPS23-linked RFP was performed in HEK293 using Lipofectamine 2000 (Invitrogen). The induced expression of HA-tagged TTP and myc-tagged HuR were used as outlined previously (4,5,21).…”

Section: Are Reporter Constructs and Transfectionmentioning

confidence: 99%

“…Total RNA was extracted (TRI reagent, Sigma) and reverse transcribed as described previously (5). qPCR was performed in multiplex using FAM-labeled TaqMan primer and probe sets (Applied Biosystems) as outlined in Supplementary Methods, and normalized to VIC-labeled human GAPDH or RPLPO as the endogenous control.…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

“…Western blotting was performed as described previously (5). Specific antibodies to TTP, HuR, and serine phosphorylated H3 histone were obtained from Santa Cruz Biotechnology.…”

Section: Western Blottingmentioning

confidence: 99%

“…A growing body of evidence has linked aberrantly elevated and prolonged expression of ARE-encoding mRNAs to cancer, including those participating in angiogenesis, chemotaxis, and invasion. Examples of such genes include EGF, estrogen receptor (ER), COX-2, VEGF, matrix metalloproteinase (MMP) 1, the chemokine receptor CXCR4, and urokinase-type plasminogen activator (uPA) and its receptor (4)(5)(6)(7)(8)(9). The ARE-mRNAs are regulated by trans-acting RNA-binding proteins notably tristetraprolin (TTP/ZFP36) and human antigen R (HuR/ELAVL1).…”

Section: Introductionmentioning

confidence: 99%

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Systematic Analysis of AU-Rich Element Expression in Cancer Reveals Common Functional Clusters Regulated by Key RNA-Binding Proteins

et al. 2016

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Interleukin‐4‒induced posttranscriptional gene regulation of CCL26 by the RNA‐binding protein HuR in primary human nasal polyp‒derived epithelial cells

Tian

et al. 2018

Int Forum Allergy Rhinol

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Background: Much a ention on the pathophysiology of nasal polyp (NP) has focused on eosinophils. Interleukin (IL)-4 and eotaxin-3 (C-C motif chemokine ligand 26, or CCL26) levels have been reported to be increased in eosinophilic nasal polyps. The aim of this study was to characterize CCL26 pos ranscriptional regulation by the RNAbinding protein HuR in primary human nasal polyp-derived epithelial cells (hNPDECs) challenged with IL-4. Methods:A prospective, observational study was conducted. Nasal polyp tissues were obtained from eosinophilic (n = 12) and non-eosinophilic (n = 10) NP patients, and inferior turbinate (IT) tissues were taken from control subjects (n = 9) and cultured into hNPDECs. Expression of HuR and CCL26 were measured by immunohistochemistry, Western blot analysis, enzyme-linked immunoassay, and real-time polymerase chain reaction (PCR). The nucleocytoplasmic shu ling of HuR in hNPDECs was detected by immunofluorescence. Pos ranscriptional regulation of CCL26 by HuR was tested by ribonucleoprotein immunoprecipitation assay (RIP) and dual-luciferase reporter assay. CCL26 mRNA stabilization was measured by quatititative PCR a er treatment with actinomycin D. Student's t test and one-way analysis of variance were used.Results: Immunohistochemical data show that both HuR and CCL26 were highly expressed in NP tissues, especially eosinophilic NP tissues (p < 0.05). IL-4 stimulation increased CCL26 mRNA stability, and overexpression and knockdown of HuR affected CCL26 expression. Immunofluorescence data indicate that IL-4 altered the subcellular distribution of HuR. The RIP and dual-luciferase reporter assay results supply strong evidence for HuR binding to CCL26. Conclusion:Our results provide strong support for the hypothesis that IL-4-induced expression of CCL26 in hN-PDECs relies partly on CCL26 mRNA stabilization mediated by the interaction of HuR with CCL26 3'UTR. C 2018 ARS-AAOA, LLC.

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Posttranscriptional control of the chemokine receptor CXCR4 expression in cancer cells

Abstract: SummaryWe demonstrate that CXCR4 mRNA contains ARE in its 3′-UTR and regulated by the RNA-binding proteins, TTP and HuR. Normalization of the aberrant TTP-HuR axis resulted in reduced invasion and migration of breast cancer cells toward CXCL12.

Cited by 35 publications

References 47 publications

The role of adhesion molecules in acute myeloid leukemia and (hemato)oncology: A systematic review

The role of adhesion molecules in acute myeloid leukemia and (hemato)oncology: A systematic review

Systematic Analysis of AU-Rich Element Expression in Cancer Reveals Common Functional Clusters Regulated by Key RNA-Binding Proteins

Interleukin‐4‒induced posttranscriptional gene regulation of CCL26 by the RNA‐binding protein HuR in primary human nasal polyp‒derived epithelial cells

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