Relationship Between Mef4 And Nucleophosmin

Good Essays
The main objective of this paper by Ando et al. was to explore the nature of association between the protein MEF/ELF4 and the nucleophosmin, NPM1, along with its implications with regards to leukemogenesis; the mutant version of the latter has been commonly associated with leukemia.
MEF/ELF4 is part of a family of transcriptional factors (ETS) responsible for numerous cellular functions, such as genomic stability, DNA repair, and most importantly, the regulation of cell proliferation, differentiation and cell death. In particular, MEF/ELF4 is expressed in hematopoietic cells in order to control their movement through the eukaryotic cell cycle, thus classifying it as a potential oncogene. Previous studies have demonstrated that the human HDM2 promoter is a target of the MEF transcriptional factor and the overexpression of MEF led to an increase in the Mdm2 protein (mice version of the human Hdm2), which in turn decreased the expression of the tumor-suppressor, p53, thereby augmenting transformation that may lead to leukemogenesis. Furthermore, the mutation commonly found in leukemia patients resulted in the delocalization of the NPM1 protein from the nucleolus to the
…show more content…
Not only that, but this paper also includes a variety of techniques, some of which are unfamiliar, thus, providing me with the chance to learn. Moreover, the choice to include multiple techniques to prove one main point makes the author’s conclusions more convincing, as all of their assays worked in synergy. The findings of this paper may be able to suggest potential gene therapies for leukemia patients with normal karyotype but mutated NPM1 gene. Perhaps, siRNA targeted against the mutated gene or its restoration can inhibit NPM1’s aberrant expression in the cytoplasm. Since the mutation results in a nucleotide gain at the C termini, the truncation and subsequent re-folding of the protein may be able to restore its wild type

Related Documents

  • Decent Essays

    ATF3 function in cancer cells: oncogene vs. tumor suppressor The mouse homolog of ATF3 (named TI-241) was identified by differential hybridization due to its high expression in the extremely metastatic melanoma cell line B16-F10, and absence in the related but non-metastatic cell line B16-F1. While characterizing the ATF3 mouse homolog, it was found that over-expression of ATF3 in the non-metastatic B16-F1cells converted them into highly metastatic cells, therefore, suggesting that ATF3 functions as an oncogene in melanoma. Subsequently, the same group described an oncogenic role of ATF3 in a human colon cancer cell line; wherein knock-down of ATF3 in the cancer cells reduced tumor growth in vivo and increased survival of the mice. However,…

    • 1213 Words
    • 5 Pages
    Decent Essays
  • Decent Essays

    To examine whether these candidates are also altered in pancreatic ASC, I will analyze the RNA levels of top targets in pancreatic ASC samples that contain UPF1 mutations. To determine the function of the identified candidates from high-throughput sequencing, I will perform overexpression and knockdown experiments in primary pancreatic cell lines to examine for corresponding gain or loss in proliferation. In addition, I will determine whether overexpression of the candidates transforms primary pancreatic cells. In summary, results from this aim will elucidate the mechanism by which UPF1 mutations promote pancreatic…

    • 1047 Words
    • 4 Pages
    Decent Essays
  • Decent Essays

    These steps include dendritic cells promoting tumor antigens obtained from tumor microenvironments or dead tumor cells, recruitment of activated T-cells to cause responses and circumventing immunosuppression in the tumor microenvironment (Kershaw, Devaud et. 2013). Dendritic cells can present antigens using MHC class I and II molecules by moving to the lymph nodes to expose antigens to T cells upon receiving a stimulus (Vegh , Wang et. 1993). The activated naïve T cells can migrate to region containing antigens and target cancer cells displaying these antigens.…

    • 1172 Words
    • 5 Pages
    Decent Essays
  • Decent Essays

    Adaptive Immune Response

    • 785 Words
    • 4 Pages

    B cells express specific antigen receptors (immunoglobulin molecules) on their cell surface during their development and, when mature in the bone marrow, secrete soluble immunoglobulins (antibodies) into the extracellular fluids. Each B cell is genetically programmed to express a surface receptor…

    • 785 Words
    • 4 Pages
    Decent Essays
  • Decent Essays

    The benefit of these drugs is that it can work in all phases of the cell cycle. One downside to using Anti-tumor antibiotics is that high doses can be linked to heart damage. Topoisomerase inhibitors conflict with enzymes like Anti-tumor antibiotics. This is done to detached the strands of DNA that would be imitated. Common cancers Topoisomerase inhibitor drugs treat are leukemia, lung, and ovarian cancers.…

    • 1072 Words
    • 5 Pages
    Decent Essays
  • Decent Essays

    Explain how changes in the following three types of genes can cause cancer ○ Explain the role of Tumor Suppressor Genes when functioning normally. The tumor suppressor gene controls Ras genes and P53, it slows cell division ○ What are the mutations that can occur in those genes? Missense, Nonsense, Deletion, Insertion, Substitution, Inversion, Duplication ■ How do those mutations cause cancer? Chromosome rearrangements: Changes in chromosomes that put one gene next to another, which allows one gene to activate the other Gene duplication: Having extra copies of a gene, which can lead to it making too much of a certain protein ■ Provide 2 common examples Familial retinoblastoma: occurs when a baby inherits from one of its parents a chromosome (number 13) that has its RB locus deleted. The normal Rb protein controls the cell cycle.…

    • 1004 Words
    • 5 Pages
    Decent Essays
  • Decent Essays

    This section is the primary focus of my paper and is a target principle in my focus question: signaling pathways specifically the Wnt-beta catenin pathway. This topic gives lots of information on the development of cancer and how cancer stem cells differ from cancer cells and stem…

    • 1133 Words
    • 5 Pages
    Decent Essays
  • Decent Essays

    When the DNA is damaged, it automatically activates the p53 gene. p53 or usually known as a tumor protein, attaches to miR-34a promoter in order to normalize the expression of microRNAs. p53 eliminates the opportunity for a tumor to occur in correlation with transcriptional targets and having miR-34a to the side in order to avoid any inappropriate cell propagation. Likewise, any damage in the DNA signaling could affect the evolutionary biogenetics process from the p53 gene activation. MicroRNA-34a together with p53, activate SIRT-1, a protein that catalyzes NAD- dependent deacetylation (Rahman, 2011).…

    • 2340 Words
    • 10 Pages
    Decent Essays
  • Decent Essays

    The surface of the EC also contains thrombomodulin which activates protein C and S. Also the EC can produce tissue- and urokinase- type plasminogen activators which activate plasminogen into plasmin. (Fig.1) ECs are originated from a common origin known as blood islands in the embryo’s periphery.1 Arterial Smooth muscle cells: Smooth muscle cell (SMC) is the second major cell type of the normal artery. These cells contract and relax thus controlling…

    • 962 Words
    • 4 Pages
    Decent Essays
  • Decent Essays

    The Cause Of Cancer

    • 1239 Words
    • 5 Pages

    The certain mutations required for detection, signaling, and repair of DNA damage can actually lead to more DNA damage, the incorrect repair of damage, and cancer. If DNA repair pathways that are needed for the life and growth of a tumor can be found and delayed, then the use of chemotherapy and radiotherapy can and will be much more successful (Bolderson, Richard, Zhou, and Khanna,…

    • 1239 Words
    • 5 Pages
    Decent Essays

Related Topics