Primary Faculty Mentor Name

Frances Carr, Ph.D.

Project Collaborators

Noelle Gillis (Graduate Student Mentor), Eric Bolf (Graduate Student Mentor), Jennifer Tomczak (Lab Technician)

Graduate Student Mentors

Noelle Gillis, Eric Bolf

Status

Undergraduate

Student College

College of Agriculture and Life Sciences

Program/Major

Microbiology

Primary Research Category

Health Sciences

Presentation Title

The Role of Estrogen Receptor Alpha (ERα) in Thyroid Tumorigenesis

Time

1:00 PM

Location

Silver Maple Ballroom - Health Sciences

Abstract

Thyroid cancer is three times more prevalent in females than males, and its incidence for females has risen almost 4% annually over the past few decades. 17β-estradiol (E2) is a recognized growth promoter and Group 1 carcinogen, and its signaling is largely mediated by estrogen receptors alpha (ERα) and beta (ERβ). While ERβ’s role is unclear, ERα is shown to be oncogenic in breast and ovarian cancers. Runt-related transcription factor 2 (RUNX2) is a recognized oncogene linked to tumor invasion and metastasis of thyroid carcinoma. Thyroid hormone receptor beta (TRβ) is a tumor suppressor, and the Carr lab revealed a novel signaling pathway by which TRβ suppresses RUNX2 expression. ERα is present in thyroid tissue, and is shown to increase RUNX2 levels and metastatic activity in breast cancer. With tumor suppressor TRβ and tumor promoter ERα sharing overlapping response elements in the promoter of RUNX2, a compelling question is whether there exists a relationship between these transcriptional regulators in thyroid tumorigenesis. We first seek to elucidate ERα’s role in thyroid cancer. Here, we determine basal expression for ERα and ERβ across thyroid cell lines spanning the spectrum of thyroid cancer (both highest in “normal” thyroid cells). We show that ERα binds to the promoter of RUNX2 in “normal” cells treated with E2 by chromatin immunoprecipitation. Overexpression of ERα in “normal” cells treated with physiological E2 within a 24-hour period significantly increased RUNX2 expression, but did not significantly affect expressions of a RUNX2 target, proliferation markers, nor EMT markers. These findings indicate that more research into this subject is required. However, if ERα and TRβ work in an opposing manner in thyroid tumorigenesis, this would open up the opportunity for improving diagnostic exams and developing novel treatment methods.

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The Role of Estrogen Receptor Alpha (ERα) in Thyroid Tumorigenesis

Thyroid cancer is three times more prevalent in females than males, and its incidence for females has risen almost 4% annually over the past few decades. 17β-estradiol (E2) is a recognized growth promoter and Group 1 carcinogen, and its signaling is largely mediated by estrogen receptors alpha (ERα) and beta (ERβ). While ERβ’s role is unclear, ERα is shown to be oncogenic in breast and ovarian cancers. Runt-related transcription factor 2 (RUNX2) is a recognized oncogene linked to tumor invasion and metastasis of thyroid carcinoma. Thyroid hormone receptor beta (TRβ) is a tumor suppressor, and the Carr lab revealed a novel signaling pathway by which TRβ suppresses RUNX2 expression. ERα is present in thyroid tissue, and is shown to increase RUNX2 levels and metastatic activity in breast cancer. With tumor suppressor TRβ and tumor promoter ERα sharing overlapping response elements in the promoter of RUNX2, a compelling question is whether there exists a relationship between these transcriptional regulators in thyroid tumorigenesis. We first seek to elucidate ERα’s role in thyroid cancer. Here, we determine basal expression for ERα and ERβ across thyroid cell lines spanning the spectrum of thyroid cancer (both highest in “normal” thyroid cells). We show that ERα binds to the promoter of RUNX2 in “normal” cells treated with E2 by chromatin immunoprecipitation. Overexpression of ERα in “normal” cells treated with physiological E2 within a 24-hour period significantly increased RUNX2 expression, but did not significantly affect expressions of a RUNX2 target, proliferation markers, nor EMT markers. These findings indicate that more research into this subject is required. However, if ERα and TRβ work in an opposing manner in thyroid tumorigenesis, this would open up the opportunity for improving diagnostic exams and developing novel treatment methods.