ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY

ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY

Bibliographic Details
Main Author: Smigiel, Jacob
Language:English
Published: Case Western Reserve University School of Graduate Studies / OhioLINK 2018
Subjects:
Cellular Biology
Tumor Microenvironment
Oncostatin M
STAT3-SMAD3
Cell Plasticity
Online Access:http://rave.ohiolink.edu/etdc/view?acc_num=case152891618991579
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spelling ndltd-OhioLink-oai-etd.ohiolink.edu-case1528916189915792021-08-03T07:07:10Z ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY Smigiel, Jacob Cellular Biology Tumor Microenvironment Oncostatin M STAT3-SMAD3 Cell Plasticity Metastasis and disease recurrence following therapy failure are the driving forces behind patient mortality associated with cancer. Pancreatic ductal adenocarcinoma (PDAC) and triple negative breast cancer (TNBC) are two highly aggressive diseases which are notoriously known for their metastatic dissemination, therapeutic resistance, and abysmal prognosis. Currently only generalized chemotherapy, and localized radiotherapy are the main avenues of targeting TNBC and PDAC. It stands to reason that novel targeted therapies are needed for patients suffering from TNBC and PDAC, recently our lab and others have focused on the role the tumor micro-environment (TME) plays in regulating cancer cell plasticity, that is the ability for epithelial/non-cancer stem cells to undergo a cellular reprograming to a mesenchymal/cancer stem-like cell state in response to TME cues and contribute to drug resistance or disease recurrence. Here we demonstrate how GREM1 can inhibit oncostatin M (OSM) induced cell plasticity. Furthermore, we uncover that OSM induced plasticity requires OSMR activated STAT3/SMAD3 cooperativity, a potential new avenue of therapeutically targeting cell plasticity. Finally, we discuss the possibility of divergent mesenchymal/tumor initiating programs engaged by OSMR-STAT3/SMAD3 signaling and the implications of identifying novel mechanisms involved in invasion, drug resistance, and tumor initiating capabilities. 2018-08-31 English text Case Western Reserve University School of Graduate Studies / OhioLINK http://rave.ohiolink.edu/etdc/view?acc_num=case152891618991579 http://rave.ohiolink.edu/etdc/view?acc_num=case152891618991579 unrestricted This thesis or dissertation is protected by copyright: all rights reserved. It may not be copied or redistributed beyond the terms of applicable copyright laws.
collection NDLTD
language English
sources NDLTD
topic Cellular Biology
Tumor Microenvironment
Oncostatin M
STAT3-SMAD3
Cell Plasticity
spellingShingle Cellular Biology
Tumor Microenvironment
Oncostatin M
STAT3-SMAD3
Cell Plasticity
Smigiel, Jacob
ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY
author Smigiel, Jacob
author_facet Smigiel, Jacob
author_sort Smigiel, Jacob
title ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY
title_short ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY
title_full ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY
title_fullStr ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY
title_full_unstemmed ONCOSTATIN M & TRANSFORMING GROWTH FACTOR SIGNALING CONVERGE TO REGULATE CANCER CELL PLASTICITY
title_sort oncostatin m & transforming growth factor signaling converge to regulate cancer cell plasticity
publisher Case Western Reserve University School of Graduate Studies / OhioLINK
publishDate 2018
url http://rave.ohiolink.edu/etdc/view?acc_num=case152891618991579
work_keys_str_mv AT smigieljacob oncostatinmtransforminggrowthfactorsignalingconvergetoregulatecancercellplasticity
_version_ 1719453897871851520

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