Effect of Inhibin on the Interaction of TGF-Β Receptors

School Name

Governor's School for Science & Mathematics

Grade Level

12th Grade

Presentation Topic

Cell and Molecular Biology

Presentation Type

Mentored

Mentor

Mentor: Mythreye Karthikeyan, University of South Carolina

Abstract

Members of the transforming growth factor-β (TGF-β) superfamily act to suppress or promote the progression of cancer through mechanisms that have yet to be fully validated in the scientific community. Patients with ovarian, prostate, and lung cancers, specifically, have shown higher levels of a TGF-β superfamily member known as Inhibin. However, in vivo experiments involving Inhibin null mice have suggested that Inhibin functions to suppress gonadal tumorigenesis, or the development of tumors in the gonadal area. Inquiries into the effect of Inhibin on the TGF-β pathway could lead to a better understanding of how this pathway functions in cancerous cells. The goal of this study is to discover the consequences of high Inhibin levels in cancers on a basic, mechanistic level. This was achieved by attempting to determine the interactions between TGF-β superfamily members that naturally generate dimers. The receptors combinations used were Type II Receptor ACTRII with Type I Receptor ALK1 and Type II Receptor ACTRII with coreceptor Endoglin. In this investigation, immunofluorescense staining was used to determine the distribution of receptors on the Cos7 cell surface. The numerical data derived from a count of all receptors and their colocalization points was then analyzed. On average, Inhibin increased the interaction between each pair of receptors. In the future, further research involving Inhibin and various TGF-β receptors could lead to a better understanding of the TGF- β pathway, and therefore a better understanding of cancer.

Start Date

3-25-2017 11:59 PM

Presentation Format

Written Only

Group Project

No

COinS
 
Mar 25th, 11:59 PM

Effect of Inhibin on the Interaction of TGF-Β Receptors

Members of the transforming growth factor-β (TGF-β) superfamily act to suppress or promote the progression of cancer through mechanisms that have yet to be fully validated in the scientific community. Patients with ovarian, prostate, and lung cancers, specifically, have shown higher levels of a TGF-β superfamily member known as Inhibin. However, in vivo experiments involving Inhibin null mice have suggested that Inhibin functions to suppress gonadal tumorigenesis, or the development of tumors in the gonadal area. Inquiries into the effect of Inhibin on the TGF-β pathway could lead to a better understanding of how this pathway functions in cancerous cells. The goal of this study is to discover the consequences of high Inhibin levels in cancers on a basic, mechanistic level. This was achieved by attempting to determine the interactions between TGF-β superfamily members that naturally generate dimers. The receptors combinations used were Type II Receptor ACTRII with Type I Receptor ALK1 and Type II Receptor ACTRII with coreceptor Endoglin. In this investigation, immunofluorescense staining was used to determine the distribution of receptors on the Cos7 cell surface. The numerical data derived from a count of all receptors and their colocalization points was then analyzed. On average, Inhibin increased the interaction between each pair of receptors. In the future, further research involving Inhibin and various TGF-β receptors could lead to a better understanding of the TGF- β pathway, and therefore a better understanding of cancer.