The roles of the ERK and HSP-60 in Tumorigenic Cancers: Discussing Potentially Novel Treatment Methods
Loading...
Authors
Clate, Nicholas
Wilson, Mark
Montague, Charlotte
Trosch, William
Issue Date
2023-04-28
Type
Other
Language
en_US
Keywords
Scholarship Sewanee 2023 , University of the South , HSP-60 , ERK-5 , Cancer , Neuroscience
Alternative Title
Abstract
Within the United States, tumorigenic cancers are currently a near-hopeless battle for families seeking treatment. Medulloblastoma and malignant neoplasms have a median survival rate among pediatric cases of only 3 years, and the drugs and treatment used cost up to $2900 a day and $1000 a month respectively. These treatments have significant environmental costs such as increasing the water footprint incurred by hospitals through longer use of treatment and the requirement for intensive treatment post-care. Our group selected two proteins heavily involved in the survival and proliferation of these cancers - HSP-60 and ERK.
HSP-60 is involved in the rate at which cancer metastasizes in ERK-MAPK-type cancers. This is in part due to the rates at which extracellular signaling is permitted in normal cell function due to HSP-60’s function in repairing proteins - in the case that this is downregulated the cell may enter apoptosis as it expands its energy repairing itself. HSP-60 also impacts the formation of complexes with survivin - a protein repressor of apoptosis involved in inhibiting caspase activation. In tumor cells, both proteins have been found to be overexpressed. Silencing the amount of these proteins inhibits cell proliferation and can induce apoptosis in tumor cells.
ERK is a protein involved in neural proliferation and dendrite outgrowth in neurons and has been identified as showing increased expression in various tumorigenic cancers. These cancers are known to metastasize and grow relatively fast and in most cases have poor post-treatment outlook. The ERK/MAPK pathway is also part of the deregulation of several extracellular cascades that involve cell proliferation. It also has the potential to deregulate anti-apoptotic transcription factors. Expression of ERK is most frequently identified in the later stages of cancer because at these stages ERK is continuously activated.
Utilization of current ERK and HSP-60 inhibitors is only administered through oral or IV administration methods. These administration methods have the potential for an overall loss in body mass due to their widespread effects once in the body. A solution to this could be the use of a small diffusion path-based administrative pathway, limiting the potential for negative effects on the body as a whole.
Description
Citation
Publisher
University of the South