“…It has also been indicated that GAS5 can suppress MYC expression, suggesting another mechanism through which GAS5, at least partly, induces its tumor-suppressive effect [ 96 ]. An examination of 80 newly diagnosed patients with CLL showed that low levels of LincRNA-P21 were significantly associated with poor outcomes, and that this lncRNA showed a negative correlation with CD38, ZAP70, and absolute lymphocyte count [ 117 ]. Additionally, the BM742401 methylation status was significantly associated with a higher white blood cell count and advanced Rai stage [ 118 ].…”
Section: Alterations In Lncrnas In Lymphoid Malignancymentioning
Lymphoid cells play a critical role in the immune system, which includes three subgroups of T, B, and NK cells. Recognition of the complexity of the human genetics transcriptome in lymphopoiesis has revolutionized our understanding of the regulatory potential of RNA in normal lymphopoiesis and lymphoid malignancies. Long non-coding RNAs (lncRNAs) are a class of RNA molecules greater than 200 nucleotides in length. LncRNAs have recently attracted much attention due to their critical roles in various biological processes, including gene regulation, chromatin organization, and cell cycle control. LncRNAs can also be used for cell differentiation and cell fate, as their expression patterns are often specific to particular cell types or developmental stages. Additionally, lncRNAs have been implicated in lymphoid differentiation, such as regulating T-cell and B-cell development, and their expression has been linked to immune-associated diseases such as leukemia and lymphoma. In addition, lncRNAs have been investigated as potential biomarkers for diagnosis, prognosis, and therapeutic response to disease management. In this review, we provide an overview of the current knowledge about the regulatory role of lncRNAs in physiopathology processes during normal lymphopoiesis and lymphoid leukemia.
“…It has also been indicated that GAS5 can suppress MYC expression, suggesting another mechanism through which GAS5, at least partly, induces its tumor-suppressive effect [ 96 ]. An examination of 80 newly diagnosed patients with CLL showed that low levels of LincRNA-P21 were significantly associated with poor outcomes, and that this lncRNA showed a negative correlation with CD38, ZAP70, and absolute lymphocyte count [ 117 ]. Additionally, the BM742401 methylation status was significantly associated with a higher white blood cell count and advanced Rai stage [ 118 ].…”
Section: Alterations In Lncrnas In Lymphoid Malignancymentioning
Lymphoid cells play a critical role in the immune system, which includes three subgroups of T, B, and NK cells. Recognition of the complexity of the human genetics transcriptome in lymphopoiesis has revolutionized our understanding of the regulatory potential of RNA in normal lymphopoiesis and lymphoid malignancies. Long non-coding RNAs (lncRNAs) are a class of RNA molecules greater than 200 nucleotides in length. LncRNAs have recently attracted much attention due to their critical roles in various biological processes, including gene regulation, chromatin organization, and cell cycle control. LncRNAs can also be used for cell differentiation and cell fate, as their expression patterns are often specific to particular cell types or developmental stages. Additionally, lncRNAs have been implicated in lymphoid differentiation, such as regulating T-cell and B-cell development, and their expression has been linked to immune-associated diseases such as leukemia and lymphoma. In addition, lncRNAs have been investigated as potential biomarkers for diagnosis, prognosis, and therapeutic response to disease management. In this review, we provide an overview of the current knowledge about the regulatory role of lncRNAs in physiopathology processes during normal lymphopoiesis and lymphoid leukemia.
“…Similarly, Croce and coworkers reported a strong correlation between lncRNA MIAT expression and disease aggressiveness since lncRNA upregulation protects CLL lymphocytes from apoptosis, ultimately sustaining monoclonal malignant B cell proliferation 14 . Conversely, the expression of lincRNA‐p21 is significantly reduced in CLL patients, and low expression of this lncRNA demarcates a more aggressive form of CLL with a poor prognosis 15 . LincRNA‐p21 and the paraspeckle‐enriched lncRNA NEAT1 are involved in the induction of cell death after DNA damage 16 ; however, we recently observed that the expression of NEAT1 is quite heterogeneous in B cells derived from CLL patients irrespectively of cytogenetic groups or clinical outcome 17 …”
Section: Introductionmentioning
confidence: 98%
“… 14 Conversely, the expression of lincRNA‐p21 is significantly reduced in CLL patients, and low expression of this lncRNA demarcates a more aggressive form of CLL with a poor prognosis. 15 LincRNA‐p21 and the paraspeckle‐enriched lncRNA NEAT1 are involved in the induction of cell death after DNA damage 16 ; however, we recently observed that the expression of NEAT1 is quite heterogeneous in B cells derived from CLL patients irrespectively of cytogenetic groups or clinical outcome. 17 …”
Section: Introductionmentioning
confidence: 98%
“…14 Conversely, the expression of lincRNA-p21 is significantly reduced in CLL patients, and low expression of this lncRNA demarcates a more aggressive form of CLL with a poor prognosis. 15 LincRNA-p21 and the paraspeckleenriched lncRNA NEAT1 are involved in the induction of cell death after DNA damage 16 ; however, we recently observed that the expression of NEAT1 is quite heterogeneous in B cells derived from CLL patients irrespectively of cytogenetic groups or clinical outcome. 17 LINC00152, also known as CYTOR (cytoskeleton regulator RNA), is an intergenic lncRNA initially reported to control cell cycle progression through the interaction with a network of proteins associated with the M phase of the cell cycle, thus acting as a noncoding oncogene.…”
Long non‐coding RNAs are emerging as essential regulators of gene expression, but their role in normal and neoplastic B cells is still largely uncharacterized. Here, we report on the expression pattern of the LINC00152 in normal B cells and Chronic Lymphocytic Leukemia B cell clones. Higher LINC00152 levels were consistently observed in memory B cell populations when compared to naïve B cells in the normal tissues analyzed [peripheral blood (PB), tonsils, and spleen]. In addition, independent stimulation via Immunoglobulins (IG), CD40, or Toll‐like Receptor 9 (TLR9) upregulated LINC00152 in PB B cells. The expression of LINC00152 in a cohort of 107 early stage Binet A CLL patients was highly variable and did not correlate with known prognostic markers or clinical evolution. TLR9 stimulation, but not CD40 or IG challenge, was able to upregulate LINC00152 expression in CLL cells. In addition, LINC00152 silencing in CLL cell lines expressing LINC00152 failed to induce significant cell survival or apoptosis changes. These data suggest that, in normal B cells, the expression of LINC00152 is regulated by immunomodulatory signals, which are only partially effective in CLL cells. However, LINC00152 does not appear to contribute to CLL cell expansion and/or survival in a cohort of newly diagnosed CLL patients.
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