Investigating the role of GM-CSF and Rab27a in the metastatic potential and progression of oncogenic KRAS driven PDAC
Public Deposited- Last Modified
- February 26, 2019
- Creator
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Bagchi, Sukriti
- Affiliation: College of Arts and Sciences, Department of Chemistry
- Abstract
- Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a consistently poor prognosis (<7% five-year survival rate). Oncogenic KRAS is the primary driver of PDAC, present in ~95% of cases, and has been previously shown to upregulate GMCSF, a cytokine contributing to a pro-tumorigenic, immunosuppressive microenvironment in the pancreas via MDSCs (myeloid-derived suppressor cells). Additionally, Rab27a mediated exosome secretion can also initiate a pre-metastatic niche in the liver, priming them for tumor infiltration through macrophage recruitment. In this project, stable knockdowns were generated for Rab27a in pancreatic ductal epithelial cells from KPC mice (KPC PDECs) and injected back into the pancreata of mice to determine metastatic potential. After harvesting and analyzing the livers by flow cytometry and histology, initial data shows a reduction of MDSCs but not in macrophages, suggesting a way by which Rab27a can mediate formation of a pre-metastatic niche. Stable knockdowns for GM-CSF are in the process of being generated for similar analysis.
- Date of publication
- spring 2017
- Keyword
- DOI
- Resource type
- Rights statement
- In Copyright
- Note
- Funding: None
- Advisor
- Pylayeva-Gupta, Yuliya
- Degree
- Bachelor of Arts
- Academic concentration
- Chemistry
- Honors level
- Honors
- Degree granting institution
- University of North Carolina at Chapel Hill
- Graduation year
- 2017
- Language
- English
Relations
- Parents:
This work has no parents.
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