University of Nevada - Reno
Secreted Factors from CD36+ Fibroblasts Induce Tumor Suppression in Subtypes of Breast Cancer
Abstract
dc:description.abstractHuman breast cancers are not fully autonomous. They are dependent on nutrients and growth-promoting signals provided by stromal cells. In order to instruct the surrounding cells to provide essential growth factors, cancer cells co-opt normal signaling molecules and mechanisms. To inhibit or potentially reverse tumor growth, our goal is to emulate this signaling and reprogram the microenvironment. For example, in a healthy mammary gland, fibroblasts (FBs) overexpress CD36; the downregulation of CD36 is one of the hallmarks of cancer-associated FBs. Therefore, in this project, we hypothesized that signaling from CD36+ FBs could cause growth suppression in a subset of breast cancer cell lines. We then designed a series of experiments to validate this growth suppression and elucidate secreted factors by CD36+ FBs that induce growth suppression. These experiments suggested three protein ligands of SLIT3, FBLN1, and PENK induce growth suppression in a subset of breast cancer subtypes.
Degree
thesis:*- Level thesis:degree_level
- Doctorate Degree
- Year dc:date.issued
- 2021
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Jabbari, Kosar
- Advisor dc:contributor.advisor
-
- Parvin, Bahram
- Committee members dc:contributor.committeemember
-
- Shen, Yantao
- Zhu, Xiaoshan
- Zaklit, Josette
- Alvarez-Ponce, David
Identifiers
dc:identifier.*- Handle dc:identifier.uri
- http://hdl.handle.net/11714/8051
- OAI identifier oai:identifier
- oai:scholarwolf.unr.edu:11714/8051