Shahad Hilal
Pronouns: She/Her/Hers
Research Mentor(s): Priyan Weerappuli, Postdoctoral Scholar
Research Mentor School/College/Department: Biological and Material Sciences, School of Dentistry
Presentation Date: Thursday, April 22, 2021
Session: Session 3 (1pm-1:50pm)
Breakout Room: Room 12
Presenter: 1
Abstract
Neutrophils, immune cells that fight infection, can produce neutrophil extracellular traps (NETs), which are DNA meshes of the neutrophil cell. These NETs function by trapping pathogens and aiding in the immune response. However, NETs produced by neutrophils in the tumor microenvironment can promote cancer metastasis. Breast cancer metastasis is associated with very high mortality rates, and by studying the mechanism associated with NETs in promoting breast cancer metastasis, a potential therapeutic target may be identified. Two mammary cell lines were utilized in this study: 4T1 and 4T07, of which only 4T1 tumor cells metastasize. 4T1 tumors were observed to contain greater levels of infiltrating neutrophils than 4T07 tumors, and, consistent with this idea, 4T1 tumor cells express higher amounts of the CXCL1/CXCL2 chemokines, which act to recruit neutrophils. When neutrophils were prevented from making NETs, 4T1 cells stopped metastasizing, indicating the significant role NETs play in metastasis. Due to the complexity in NET structures, DHMs (DNA-histone mesostructures) were synthesized to establish controls and simulate NETs in vitro. By culturing 4T1 and 4T07 cells with and without DHMs, we intend to produce data that may aid in identifying a mechanism through which 4T1/4T07 cells interact with NETs. We also intend to study the role Trk A, B, and C receptors play in the production of chemokines, which act as neutrophil recruiters. This may lead to the development of treatments that target the recruitment of neutrophils, and thus potentially mitigate metastasis.
Authors: Shahad Hilal, Priyan Weerappuli
Research Method: Qualitative Study
