Differential expression of <scp>BIRC</scp> family genes in chronic myeloid leukaemia – <scp>BIRC3</scp> and <scp>BIRC8</scp> as potential new candidates to identify disease progression

Głodkowska-Mrówka, Eliza; Solarska, Iwona; Mrówka, Piotr; Bajorek, Katarzyna; Niesiobedzka-Krezel, Joanna; Seferyńska, Ilona; Borg, Katarzyna; Stokłosa, Tomasz

doi:10.1111/bjh.12663

Cited by 9 publications

(9 citation statements)

References 9 publications

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“…It has been reported that BIRC8 exerts its effects by association with an inhibition of specific caspases [ 27 ]. In addition, studies have documented that BIRC8 (ILP-2) is a tumor biomarker and promotes cancer progression [ 28 , 29 ]. These results suggest that ARHGEF3 regulates cell apoptosis via control of BIRC8 expression, which is in turn involved in attenuation of caspases3-induced apoptosis in the pathogenesis of NPC.…”

Section: Discussionmentioning

confidence: 99%

The putative tumor activator ARHGEF3 promotes nasopharyngeal carcinoma cell pathogenesis by inhibiting cellular apoptosis

et al. 2016

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Nasopharyngeal carcinoma (NPC) is one of the most prevalent forms of highly invasive malignancy in Southern China and Southeast Asia. The pathogenesis of NPC is a multistep process driven by the acquisition of numerous genetic abnormalities. We investigated the potential oncogenic role of the Rho-guanine nucleotide exchange factor 3 gene, ARHGEF3, in NPC pathogenesis. Expression levels of ARHGEF3 were frequently up-regulated in NPC cell lines and tissues. In a large cohort of clinical NPC tissues high expression of ARHGEF3 was positively associated with an increased T status, distant metastasis, and a more advanced clinical stage (P < 0.05). Survival analysis revealed that ARHGEF3 expression was a significant and independent prognosis factor for NPC patients. In NPC cell lines, knockdown of ARHGEF3 was sufficient to inhibit cell growth, motility, and invasion in vitro, whereas ectopic overexpression of ARHGEF3 substantially enhanced NPC cells tumorigenesis and metastasis in vivo. Depletion of ARHGEF3 in NPC cells dramatically promoted caspase-3 induced apoptosis and an anti-apoptosis factor, BIRC8, was identified as a critical downstream target of the ARHGEF3. Our findings suggest that increased expression of ARHGEF3 plays a critical oncogenic role in NPC pathogenesis by preventing cell apoptosis through the up-regulation of BIRC8, and ARHGEF3 might be employed as a novel prognostic marker and effective therapeutic target for human NPC.

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Section: Discussionmentioning

confidence: 99%

The putative tumor activator ARHGEF3 promotes nasopharyngeal carcinoma cell pathogenesis by inhibiting cellular apoptosis

et al. 2016

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“…Imatinib was the first TKI approved, and has been considered the standard of care for more than a decade. Although the therapy with Imatinib is considered a major advance in oncology, a significant group of patients still develop drug resistance ( 32 ). Second generation compounds, namely Dasatinib and Nilotinib, are highly effective in those who fail Imatinib as well as in newly diagnosed patients ( 33 ).…”

Section: And Immune Dysfunctionmentioning

confidence: 99%

Myeloid Derived Suppressor Cells in Chronic Myeloid Leukemia

et al. 2015

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The suppression of the immune system creates a permissive environment for development and progression of cancer. One population of immunosuppressive cells that have become the focus of intense study is myeloid derived suppressor cells (MDSCs), immature myeloid cells able to induce immune-escape, angiogenesis, and tumor progression. Two different subpopulations have been identified and studied: granulocytic and monocytic MDSCs, with a different immunophenotype and immunosuppressive properties. Recently, an accumulation of both Gr-MDSCs and Mo-MDSCs cells has been found in the peripheral blood of chronic myeloid leukemia (CML) patients. They are part of the tumor clone showing BCR/ABL expression. Imatinib therapy decreases both MDSCs and arginase 1 levels to normal ones. This review will focus on actual knowledge for human MDSCs and their immunosuppressive activity in CML patients, with a critical attention to comparison of Gr-MDSCs and polymorphonuclear cells (PMNs). We will then suggest the monitoring of MDSCs in patients who have discontinued tyrosine kinase inhibitors (TKIs) therapy to evaluate if their increase could correlate with disease relapse.

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“…An increased expression of inhibitors of apoptosis (IAP) has been reported, among others, in hematological malignancies [6–11], breast cancer [12], colon cancer [13–15], stomach cancer [15, 16], lymphoma, hepatocellular carcinoma [17], head and neck cancer [18], bladder cancer [19], and others. Much attention is also devoted to the possibility of using some IAP as diagnostic and prognostic markers in neoplastic diseases [20, 21]. It has been shown that in some types of cancer, cIAP1, cIAP2, Survivin, and XIAP expression levels are associated with unfavorable prognosis.…”

Section: Introductionmentioning

confidence: 99%

Potential Involvement of BIRC5 in Maintaining Pluripotency and Cell Differentiation of Human Stem Cells

Gil-Kulik

Krzyżanowski

Dudzińska

et al. 2019

Oxidative Medicine and Cellular Longevity

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The BIRC5 gene encodes a survivin protein belonging to class III of inhibitors of apoptosis, IAP. This protein serves a dual role. First, it regulates cell death, and second, it is an important regulator of mitosis progression, although its physiological regulatory function has not been fully understood. Many studies have shown and confirmed that survivin is practically absent in mature tissues in nature, while its overexpression has been reported in many cancerous tissues. There is little information about the significance of BIRC5 expression in normal adult human stem cells. This paper presents the study and analysis of survivin expression at the transcription level using qPCR method, in hematopoietic stem cells from peripheral blood mobilized with a granulocyte growth factor, adherent cells derived from the umbilical cord, and normal bone marrow stem cells. The expression of this gene was also examined in the blood of normal healthy individuals. The results of the analysis have shown that the more mature the cells are, the lower the expression of the BIRC5 gene is. The lowest expression has been found in peripheral blood cells, while the highest in normal bone marrow cells. The more the CD34+ and CD105 cells in the tested material are, the higher the BIRC5 expression is. Stem cells from cell culture show higher BIRC5 expression. The study confirms the involvement of BIRC5 from the IAP family in many physiological processes apart from apoptosis inhibition. The possible effect of BIRC5 on cell proliferation; involvement in cell cycle, cell differentiation, survival, and maintenance of stem cells; and the possible effect of IAP on the antineoplastic properties of mesenchymal stem cells have been demonstrated. Our research suggests that BIRC5 may be responsible for the condition of stem cell pluripotency and its high expression may also be responsible for the dedifferentiation of tumor cells.

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Differential expression of BIRC family genes in chronic myeloid leukaemia – BIRC3 and BIRC8 as potential new candidates to identify disease progression

Cited by 9 publications

References 9 publications

The putative tumor activator ARHGEF3 promotes nasopharyngeal carcinoma cell pathogenesis by inhibiting cellular apoptosis

The putative tumor activator ARHGEF3 promotes nasopharyngeal carcinoma cell pathogenesis by inhibiting cellular apoptosis

Myeloid Derived Suppressor Cells in Chronic Myeloid Leukemia

Potential Involvement of BIRC5 in Maintaining Pluripotency and Cell Differentiation of Human Stem Cells

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