BIOMED Home >> | Who We Are | Faculty | Research | Undergraduate Program | Graduate Programs | Students | Alumni  | Contact Us

Print friendly version of this event. Mail this event to a friend.


Master's Thesis Defense - Augmentation of a Knit Structure with Increased Suture Retention and Poly Glycerol Sebacate Coating for Rotator Cuff Repair Graft Applications

Ph.D. Thesis Defense - Impact of Envelope Cholesterol and Spike GP41 on Cell-Independent Lytic Inactivation of HIV-1 by Peptide Triazole Thiols

Master's Thesis Defense - In Vitro and Ex Vivo Substrate Stiffness Effects on Endothelial Monolayer Permeability in Response to TNF-α

Master's Thesis Defense - Determining HIV-1 Quasispecies Genomic Variability to Optimize gRNA Excision Using the CRISPR/Cas9 Gene Editing System

Master's Thesis Defense - Extending the Glue Visualization Tool with Biological Data Types

Seminar - Microstructure and Mechanical Behavior of Bone Tissue

EVENTS Archive
Master's Thesis Defense - Epidermal Growth Factor (EGF) and Transforming Growth Factor (TGFβ1) Promotes EMT in Primary Prostate Cancer Cells via Ras Signaling
Date: June 22, 2010
Time: 9:00 AM
Location: New College Building, Room: 6101

Devika Varma
Advisors: Peter Lelkes, Ph.D., Anat Katsir, Ph.D., and Mark Stearns, Ph.D.

Epidermal Growth Factor (EGF) and Transforming Growth Factor (TGFβ1) Promotes EMT in Primary Prostate Cancer Cells via Ras Signaling. Inhibitory Effects of EGCG on EMT Induced Matrix Metalloproteinase (MMP) Activity in Prostate Cancer Cells.

Epithelial to mesenchymal transition (EMT) may be a critical step in prostate cancer progression and metastasis. However, we do not understand the ligands and conditions controlling EMT. We have examined the factors controlling EMT in primary prostate cell lines isolated from human prostate cancer (i.e. IBC-10a and PCa-20a cells). We have shown that a combination of EGF and TGFβ1 (E+T) can promote expression of vimentin and matrix metalloproteinases (MMP-2/9) during induction of EMT in the primary cell lines. We have found that an intact Ras signaling was essential for E+T induced EMT. We have stably transfected IBC-10a cells with pBABE.ras constructs containing three distinct ras mutations (i.e., C40, G37 and S35). In cells transfected with C40 and S35, TGFβ1 alone induced MMP-2/9 secretion, whereas, E+T was essential to induce MMP-2/9 secretion in G37 transfected cells (i.e., which activates RalGDS and blocks Akt-1 and MEK signaling). Taken together, the data have shown, for the first time, that E+T activation of Akt-1 and MEK signaling pathways play a key role in EMT. One added goal of the study was to identify potential therapeutic agents which can block EMT. We have found that the green tea extract, Epigallocatechin-3-gallate (EGCG), blocks E+T induced MMP secretion in a dosage dependent manner in both the primary cell lines and malignant PC-3ML tumor cells. In sum, our work has demonstrated that specific ligands regulate EMT and that an herbal tea extract has potential therapeutic benefit in blocking ligand dependent EMT.


The New College Building is located at 245 N. 15th Street (15th & Race), and can be reached from main campus via the Dragon Route shuttle that boards at 33rd and Market.

Phone 215.895.2215 | Fax 215.895.4983 | Email
Copyright 2015, Drexel University, All Rights Reserved.