Daeho Kim
Pronouns: He/Him/His
UROP Fellowship: Biomedical and Life Sciences
Research Mentor(s): Zeribe Nwosu, PhD
Molecular & Integrative Physiology; Surgery
Presentation Date: Monday, July 27, 2020 | Session 1 | Presenter: 3
Authors: Daeho Kim, Zeribe C. Nwosu, Marina Pasca di Magliano
Abstract
Background: Pancreatic cancer is the third leading cause of cancer deaths. Gemcitabine is one of the main drugs used for pancreatic cancer therapy, and acts by disrupting DNA replication. However, some pancreatic cancer cell lines develop resistance to gemcitabine making the treatment ineffective. Here we aimed to determine molecular differences between gemcitabine resistant and sensitive cell lines.
Methods: We analyzed the cancerrxgene portal to determine cell lines that are either sensitive or resistant to gemcitabine. Using the NCBI GEO2R tool, we determined the differentially expressed genes between the sensitive and resistant cells. Subsequently, we used DAVID platform to perform pathway enrichment and gene ontology analyses of the differential genes.
Results: We found that pancreatic cancer cell lines AsPC-1, CAPAN-2, Hs-766T, and PANC-08-13 are resistant to gemcitabine when compared to CFPAC-1, HuP-T4, KP-4, PANC-03-27, and PSN1 (sensitive). Genomic analysis showed that topmost genes upregulated in the four resistant cell lines included BMP4, GDA, SMAD4, and MTAP, whereas top down regulated included BNIP3, NETO2, BCAT1, and EDIL3. Pathway annotation analysis showed that metabolic pathways and ubiquitin-mediated proteolysis was among upregulated pathways, whereas spliceosome and RNA transport were downregulated.
Conclusions: Our integrative application of bioinformatics tools has revealed gene expression, pathway enrichment, gene ontology, and metabolite differences between gemcitabine resistant and sensitive cell lines. These insights are the basis of subsequent experimental tests.
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Research Disciplines
Biomedical Sciences
