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Role of GRM1 in exosome production and melanoma metastasis
Descriptive
TitleInfo
Title
Role of GRM1 in exosome production and melanoma metastasis
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Isola
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Allison L.
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Allison L. Isola
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author
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Helmut
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Helmut Zarbl
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Advisory Committee
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chair
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Chen
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Suzie
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Suzie Chen
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Advisory Committee
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internal member
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White
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Lori A
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Lori A White
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Advisory Committee
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internal member
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Furmanski
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Philip
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Philip Furmanski
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Advisory Committee
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internal member
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Goydos
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James S
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James S Goydos
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Advisory Committee
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outside member
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Rutgers University
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School of Graduate Studies
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theses
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2017
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2017-10
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2017
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xx
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eng
Abstract
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Exosomes are naturally occurring membrane-bound nanovesicles generated constitutively and released by various cell types, and often in higher quantities by tumor cells. Exosomes have been postulated to facilitate communication between the primary tumor and its local microenvironment, supporting cell invasion and other early events in metastasis. A neuronal receptor, metabotropic glutamate receptor 1 (GRM1), when ectopically expressed in melanocytes, induces in vitro melanocytic transformation and spontaneous malignant melanoma development in vivo in a transgenic mouse model. Earlier studies showed that genetic modulation in GRM1 expression by siRNA or disruption of GRM1-mediated glutamate signaling by pharmacological inhibitors interfering with downstream effectors resulting in a decrease in both cell proliferation in vitro and tumor progression in vivo, suggesting that active GRM1 may participate in melanomagenesis in our system. The overall goal of this dissertation is to determine whether the presence and activation of GRM1 plays a role in exosome formation, and subsequent tumor development and progression. To test this, the first aim utilized in vitro cultured cells in which GRM1 expression and function were modulated by pharmacological and genetic means and consequences on exosome production by such manipulations were evaluated in vitro. We also assessed if exosomes derived from GRM1 expressing melanoma cells promote cell growth, migration, invasion as well as colony formation under anchorage-independent growth condition of GRM1 negative cells. Results showed that GRM1 expression in cells, per se, did not modulate exosome quantity, however, modified the qualities and functions of these exosomes. In Aim 2 we used riluzole, a glutamate signaling blockade, in a melanoma prone mouse model (TGS) for the in vivo assessment of exosomal quantity and quality. Daily treatment of TGS mice with riluzole had no detectable effect on the quantity of exosomes in circulation, however riluzole treatment influenced the effects of the circulating exosomes on metastatic behavior of recipient cells.
Subject
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Topic
Toxicology
Subject
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Topic
Melanoma
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Rutgers University Electronic Theses and Dissertations
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ETD_8304
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electronic resource
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application/pdf
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text/xml
Extent
1 online resource (x, 119 p. : ill.)
Note
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Ph.D.
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Includes bibliographical references
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by Allison L. Isola
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School of Graduate Studies Electronic Theses and Dissertations
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rucore10001600001
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NjNbRU
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doi:10.7282/T3GX4FPM
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ETD doctoral
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Rights
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The author owns the copyright to this work.
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Name
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Isola
GivenName
Allison
MiddleName
L.
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Type
Permission or license
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2017-08-23 14:16:28
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Name
Allison Isola
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Affiliation
Rutgers University. School of Graduate Studies
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Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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2017-10-31
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2019-10-31
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Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 31st, 2019.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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windows xp
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2017-08-23T20:33:10
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2017-08-23T20:33:10
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