Location

Nessmith-Lane Atrium

Session Format

Poster Presentation

Research Area Topic:

Natural & Physical Sciences - Biology

Co-Presenters, Co- Authors, Co-Researchers, Mentors, or Faculty Advisors

Ashley Williams (Georgia Southern University)

Louise Zehr (Georgia Southern University)

Vinoth Sittaramane (Georgia Southern University)

Abstract

Cancer research is a large topic in science, because over 14 million people are diagnosed worldwide, and of those, 8 million will die annually. Traditional therapies are the mainstays of treatment strategies, but a cure less invasive or with less side effects have not yet been identified. In order to develop a better cure, we need to understand the tumor and molecules present in its tissues. Integrins, cell surface proteins that aid in cell communication, have been found in the tumor tissues of several types of cancers, including prostate and neuroblastomas. Integrin alpha-6 (ITGA6), in particular, has been found to have a large effect on the progression of tumor development. In tumor tissues, we have seen an overexpression of the ITGA6 that leads to progression of tumor development. To develop a therapeutic strategy, it is important to understand the role of ITGA6 in tumor development. Using a humanized zebrafish model, we hypothesized that increasing ITGA6 will increase tumor development. To study this question, we overproduced ITGA6 by injecting human ITGA6 RNA and reduced the gene using the morpholinos. Embryos with increased ITGA6 had 27% more tumor development than embryos with reduced ITGA6. In in vitro assays, ITGA6 shows a cleaving mechanism that may contribute to tumor production. To understand the role of ITGA6 cleavage in an in vivo system, we hypothesized tumor tissues with cleaved ITGA6 will have increased tumor development. We saw that embryos with cleaved ITGA6 had 15% more tumor progression than non-cleaved ITGA6 embryos. The preliminary results support the hypothesis that increased upregulated ITGA6 and cleaved ITGA6 lead to increased tumor production. Further experiments aimed to help understand ITGA6's role in tumor progression is ITGA6 gene manipulations in the cancer cells and using these conclusions to develop a good drug screen.

Keywords

Georgia Southern University, Research Symposium, ITGA6, Integrins, Tumor development

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.

Presentation Type and Release Option

Presentation (Open Access)

Start Date

4-16-2016 10:45 AM

End Date

4-16-2016 12:00 PM

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Apr 16th, 10:45 AM Apr 16th, 12:00 PM

Investigating the Role of ITGA6 in Tumor Development

Nessmith-Lane Atrium

Cancer research is a large topic in science, because over 14 million people are diagnosed worldwide, and of those, 8 million will die annually. Traditional therapies are the mainstays of treatment strategies, but a cure less invasive or with less side effects have not yet been identified. In order to develop a better cure, we need to understand the tumor and molecules present in its tissues. Integrins, cell surface proteins that aid in cell communication, have been found in the tumor tissues of several types of cancers, including prostate and neuroblastomas. Integrin alpha-6 (ITGA6), in particular, has been found to have a large effect on the progression of tumor development. In tumor tissues, we have seen an overexpression of the ITGA6 that leads to progression of tumor development. To develop a therapeutic strategy, it is important to understand the role of ITGA6 in tumor development. Using a humanized zebrafish model, we hypothesized that increasing ITGA6 will increase tumor development. To study this question, we overproduced ITGA6 by injecting human ITGA6 RNA and reduced the gene using the morpholinos. Embryos with increased ITGA6 had 27% more tumor development than embryos with reduced ITGA6. In in vitro assays, ITGA6 shows a cleaving mechanism that may contribute to tumor production. To understand the role of ITGA6 cleavage in an in vivo system, we hypothesized tumor tissues with cleaved ITGA6 will have increased tumor development. We saw that embryos with cleaved ITGA6 had 15% more tumor progression than non-cleaved ITGA6 embryos. The preliminary results support the hypothesis that increased upregulated ITGA6 and cleaved ITGA6 lead to increased tumor production. Further experiments aimed to help understand ITGA6's role in tumor progression is ITGA6 gene manipulations in the cancer cells and using these conclusions to develop a good drug screen.