Education & Certifications
Bachelor of Arts, University of Chicago, Biological Sciences (2012)
In addition to genetic abnormalities, such as chromosomal translocations and somatic mutations that have been widely acknowledged in the leukemogenesis of acute myeloid leukemia (AML), epigenetic modifications also play a vital role in this process. MicroRNA (miRNA) regulation is emerging as a new layer of epigenetic regulation besides DNA methylation and histone modifications. Among the miRNAs first identified to be specifically expressed in hematopoietic cells, the miR-181 family has been implicated in regulating the differentiation of B cells, T cells, and natural killer cells during normal hematopoiesis, and has been linked tightly to the pathogenesis and prognosis of AML. Accumulating evidence indicates that miR-181 acts as a tumor suppressor in the pathogenesis of AML and exhibits a significant impact on the survival of patients with AML. Herein, we review the role of miR-181 as a diagnostic marker and prognostic predictor in AML, and discuss the potential use of miR-181 as a therapeutic target for AML.
View details for DOI 10.1016/j.cancergen.2014.12.006
View details for PubMedID 25686674
View details for PubMedCentralID PMC4466067
The Adenomatous Polyposis Coli (APC) tumor suppressor has been previously implicated in the control of apical-basal polarity; yet, the consequence of APC loss-of-function in epithelial polarization and morphogenesis has not been characterized. To test the hypothesis that APC is required for the establishment of normal epithelial polarity and morphogenesis programs, we generated APC-knockdown epithelial cell lines. APC depletion resulted in loss of polarity and multi-layering on permeable supports, and enlarged, filled spheroids with disrupted polarity in 3D culture. Importantly, these effects of APC knockdown were independent of Wnt/?-catenin signaling, but were rescued with either full-length or a carboxy (c)-terminal segment of APC. Moreover, we identified a gene expression signature associated with APC knockdown that points to several candidates known to regulate cell-cell and cell-matrix communication. Analysis of epithelial tissues from mice and humans carrying heterozygous APC mutations further supports the importance of APC as a regulator of epithelial behavior and tissue architecture. These data also suggest that the initiation of epithelial-derived tumors as a result of APC mutation or gene silencing may be driven by loss of polarity and dysmorphogenesis.
View details for DOI 10.1016/j.bbamcr.2014.12.036
View details for Web of Science ID 000349878500016
View details for PubMedID 25578398
View details for PubMedCentralID PMC4327896