The oncogenic potential of APOBEC3G gene was recently appreciated by the finding that revealed inhibitory influence of APOBEC3G upon micro-RNA mediated repression of the gene responsible for hepatic metastasis. Here we report for the first time that sustained APOBEC3G expression is the characteristic trait exhibited by various cancer cells of different tissue origins as well as APOBEC3G represses cellular gene coding for tumor suppressor KLF4 by binding to its mRNA. This phenomenon was paralleled by the sustained expression of the cellular SP1 which ensured overexpression of genes coding for c-myc, Bmi-1, BCL-2 and MDM2 coupled with downregulation of tumor suppressor p53 thereby creating a favorable situation for oncogenic transformation.
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http://dx.doi.org/10.1016/j.bcmd.2015.07.009 | DOI Listing |
Alzheimers Dement
December 2024
Medical University of South Carolina, Charleston, SC, USA.
Background: Alzheimer's disease (AD) is associated with cognitive impairment and neuro-inflammation. Dysregulated activation of microglia and astrocytes induces neuro-inflammation, and reactive astrocytes have been classified into A1 neurotoxic and A2 neuroprotective phenotypes. A1 astrocytes are induced by activated neuro-inflammatory microglia via secreting IL-1α, TNFα and C1q, and contributing to inflammation and neuronal cell death.
View Article and Find Full Text PDFEMBO Rep
January 2025
Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
The Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNALP) is essential for the immortalization of naive B lymphocytes (NBLs). However, the mechanisms remain elusive. To understand EBNALP's role in B-cell transformation, we compare NBLs infected with wild-type EBV and an EBNALP-null mutant EBV using multi-omics techniques.
View Article and Find Full Text PDFNat Immunol
January 2025
Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
The inflammasome plays multifaceted roles in cancer, but less is known about its function during premalignancy upon initial cell transformation. We report a homeostatic function of the inflammasome in suppressing malignant transformation through Ras inhibition. We identified increased hematopoietic stem cell (HSC) proliferation within the bone marrow of inflammasome-deficient mice.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Suite 523, Bridgeside Point II, 450 Technology Drive, Pittsburgh, PA, 15219, USA.
Overexpression of the myeloid Src-family kinases Fgr and Hck has been linked to the development of acute myeloid leukemia (AML). Here we characterized the contribution of active forms of these kinases to AML cell cytokine dependence, inhibitor sensitivity, and AML cell engraftment in vivo. The human TF-1 erythroleukemia cell line was used as a model system as it does not express endogenous Hck or Fgr.
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