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Articles 1 - 7 of 7
Full-Text Articles in Life Sciences
Understanding The Kinomic Contributions To Tyrosine Kinase Inhibitor Resistance In Triple Negative Breast Cancer, Cory Lefebvre
Understanding The Kinomic Contributions To Tyrosine Kinase Inhibitor Resistance In Triple Negative Breast Cancer, Cory Lefebvre
Electronic Thesis and Dissertation Repository
Resistance to tyrosine kinase inhibitors (TKIs) presents a growing challenge in the development of therapeutic targets for cancers such as triple negative breast cancer (TNBC), where conventional therapies are ineffective at combatting systemic disease. Potential targets in TNBC include the receptor tyrosine kinases EGFR (epidermal growth factor receptor) and c-Met, however, targeted anti-EGFR and anti-c-Met therapies have faced challenges in clinical trials due to acquired resistance. We hypothesize that response versus resistance of triple negative breast cancer to the tyrosine kinase inhibitors erlotinib and cabozantinib is mediated by compensatory changes in the kinome and phosphoproteome. To test this, we (1) …
Kindlin-1 Is Involved In Spreading, Migration, And Protein Regulation In Epidermal Scc-13 Cells, Naomi Mishan
Kindlin-1 Is Involved In Spreading, Migration, And Protein Regulation In Epidermal Scc-13 Cells, Naomi Mishan
Electronic Thesis and Dissertation Repository
Kindlin-1 is a scaffold protein linking the cytoskeleton to the extracellular matrix. Loss of function mutations in the FERMT1 gene (encoding Kindlin-1) cause gastrointestinal and skin defects associated with increased susceptibility to aggressive epidermal squamous cell carcinoma (SCC). This study investigated the consequences of targeted FERMT1 inactivation in the SCC-13 cell line of epidermal SCC. My studies demonstrate Kindlin-1 is not essential for SCC-13 proliferation or clonogenic potential in culture. Kindlin-1 was required for cell spreading on collagen I, but not on laminin-332, and its absence enhanced SCC-13 directional migration. Finally, I identified several proteins involved in tumor formation and …
Insights Into O-Glcnac-Mediated Regulation Of Galectin Expression And Secretion In Promyelocytic Hl-60 Cells, Adam J. Mctague
Insights Into O-Glcnac-Mediated Regulation Of Galectin Expression And Secretion In Promyelocytic Hl-60 Cells, Adam J. Mctague
Electronic Thesis and Dissertation Repository
Galectins are a family of -galactoside-binding proteins involved in cell stress responses and differentiation. Galectins are multifunctional proteins widely studied in many cell models including acute myeloid leukemia HL-60 cells where they mediate numerous intra- and extracellular functions in response to many stress-inducing stimuli. O-GlcNAcylation is a dynamic post-translational modification implicated in the regulation of many cellular diseases including cancers. The O-GlcNAc mediated expression and secretion of galectins during neutrophilic differentiation was examined in HL-60 cells. Galectin gene (LGALS), galectin protein expression, and galectin secretion were determined by RT-qPCR, immunoblotting, and ELISA, respectively. Inhibition of O-GlcNAcylation induced markers of differentiation …
Investigation Of Β5 Integrin Function In Epithelial Ovarian Cancer Cell Adhesion And Metastatic Properties Of Spheroids, Dolly Dhaliwal
Investigation Of Β5 Integrin Function In Epithelial Ovarian Cancer Cell Adhesion And Metastatic Properties Of Spheroids, Dolly Dhaliwal
Electronic Thesis and Dissertation Repository
Epithelial ovarian cancer (EOC) is the most lethal gynaecological malignancy in the developed world. EOC metastasis is unique since malignant cells detach directly from the primary tumor site into the abdominal fluid and form multicellular aggregates, called spheroids, that possess enhanced survival mechanisms while in suspension. As such, altered cell adhesion properties are paramount to EOC metastasis with cell detachment from the primary tumor, dissemination as spheroids, and reattachment to peritoneal surfaces for secondary tumor formation. These interactions play a crucial role in cell-cell and cell-extracellular matrix interactions, having implications in multiple steps of cancer progression. We previously showed that …
The Regulation Of Pannexin1 And Pannexin2 In The Skin In Health And Disease, Rafael E. Sanchez Pupo
The Regulation Of Pannexin1 And Pannexin2 In The Skin In Health And Disease, Rafael E. Sanchez Pupo
Electronic Thesis and Dissertation Repository
Pannexins (PANX1, 2, 3) are a family of channel-forming glycoproteins that mediate intracellular and paracrine signaling. In contrast to PANX2, PANX1 has been extensively investigated in the skin, modulating cell differentiation, wound healing, and melanoma development. PANX1 and PANX2 can co-exist in the same cell and form mixed channels where their glycosylation seems to regulate their intermixing. N-glycosylation and caspase cleavage have been proposed as modulators of the function of PANX1, but their effects on PANX2 are unknown. We explored the PANX2 expression in mouse skin and showed that a Panx2 splice variant (PANX2-202) is continuously expressed throughout aging skin. …
Functional Role Of Dream And Dyrk1a In High-Grade Serous Ovarian Cancer Cell Dormancy, Pirunthan Perampalam
Functional Role Of Dream And Dyrk1a In High-Grade Serous Ovarian Cancer Cell Dormancy, Pirunthan Perampalam
Electronic Thesis and Dissertation Repository
High-grade serous ovarian cancer (HGSOC) is the most common form of ovarian cancer. The majority of women are disproportionately diagnosed at an advanced stage (stage III-IV) of the disease when tumours have progressed beyond the ovaries or fallopian tubes and into the peritoneal cavity. Survival rates at late-stage are as low as 25% and chemoresistant disease recurrence is common, affecting up to 90% of patients. Multicellular clusters called spheroids contribute to dormancy, chemoresistance, and metastases and are a major challenge to treatment of HGSOC. Spheroid cells undergo reversible quiescence to evade chemotherapy in a process mediated by the mammalian DREAM …
Metabolic Reprogramming By Dna Tumour Viruses, Martin Prusinkiewicz
Metabolic Reprogramming By Dna Tumour Viruses, Martin Prusinkiewicz
Electronic Thesis and Dissertation Repository
Viruses are the etiological agents of approximately 12% of human cancers. However, only a subset of viral infections eventually progress to cancer. As obligate intracellular parasites, viruses create a host-cell environment that is amenable to virus replication. These changes to host-cell processes during infection are enacted by virally-encoded proteins that act as molecular hubs. When these processes intersect with pathways that encourage the development of cancer, such as the p53 tumour suppressor pathway, these virally-encoded molecular hub proteins function as viral oncoproteins. One major requirement of both virus infected cells and rapidly growing cancer cells is an altered metabolism that …