RUcore: Rutgers University Community Repository
Continuous expression of metabotropic glutamate receptor 1 is required for maintenance of tumorigenesis in GRM1 transformed mouse kidney epithelial cells
Descriptive
TypeOfResource
Text
TitleInfo
(ID = T-1)
Title
Continuous expression of metabotropic glutamate receptor 1 is required for maintenance of tumorigenesis in GRM1 transformed mouse kidney epithelial cells
Identifier
ETD_1638
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.000051419
Language
LanguageTerm
(authority = ISO639-2);
(type = code)
eng
Genre
(authority = marcgt)
theses
Subject
(ID = SBJ-1);
(authority = RUETD)
Topic
Microbiology and Molecular Genetics
Subject
(ID = SBJ-1);
(authority = ETD-LCSH)
Topic
Cancer cells--Proliferation
Subject
(ID = SBJ-1);
(authority = ETD-LCSH)
Topic
Carcinogenesis
Subject
(ID = SBJ-1);
(authority = ETD-LCSH)
Topic
Cancer--Treatment
Abstract
Within the United States, skin cancer has become a predominant form of cancer that occurs across all age groups, racial backgrounds, and to both genders equally. Melanoma arises from malignant melanocytes that reside within the epidermis of the skin. It is the most serious form of skin cancer, causing the most mortality among all skin cancers. Currently, due to the limited treatment options available, patients have severely reduced survival rates as the disease advances toward Stage IV. Advancements in understanding of the mechanisms of melanoma development and novel targets for treatment are in great need for patients inflicted with this devastating disease.
Metabotropic glutamate receptors are normally expressed within the central nervous system (CNS) where they use glutamate, the most abundant neural transmitter, as their natural ligand. Within the CNS, these receptors have important diversified functions ranging from mediation of slow excitatory and inhibitory responses to memory formation and neuronal development. Our lab has identified the etiological role of Metabotropic Glutamate Receptor 1 (Grm1) in melanoma development in transgene mouse models. Subsequently, our lab also detected GRM1 expression in approximately 40% of human melanomas biopsy and cell line samples. These results led us to investigate the role of GRM1 in other types of cancer.
Epithelial cancers are the abundant category of cancers to inflict humans, relating GRM1 and its possible role in solid tumors could introduce a novel target for developing cancer therapies. Since continuous expression of Grm1 was demonstrated to be required for the maintenance of the tumorigenic phenotype in Grm1-mouse melanocytes, my project is to determine whether this is true for an epithelial cell system. With the use of Grm1-transformed mouse kidney epithelial cells, an inducible tetracycline siRNA system was introduced into the cells and tested with/without the inducer, doxycycline, for the suppression of Grm1 expression levels in vitro and in vivo. The in vivo data demonstrated decreased tumor volumes in the doxycycline treatment groups, validating the decreased expression of Grm1 seen in vitro, compared to the no treatment groups. These results provide evidence that Grm1 expression is necessary to maintain the tumorigenic phenotype of Grm1 transformed cells.
Metabotropic glutamate receptors are normally expressed within the central nervous system (CNS) where they use glutamate, the most abundant neural transmitter, as their natural ligand. Within the CNS, these receptors have important diversified functions ranging from mediation of slow excitatory and inhibitory responses to memory formation and neuronal development. Our lab has identified the etiological role of Metabotropic Glutamate Receptor 1 (Grm1) in melanoma development in transgene mouse models. Subsequently, our lab also detected GRM1 expression in approximately 40% of human melanomas biopsy and cell line samples. These results led us to investigate the role of GRM1 in other types of cancer.
Epithelial cancers are the abundant category of cancers to inflict humans, relating GRM1 and its possible role in solid tumors could introduce a novel target for developing cancer therapies. Since continuous expression of Grm1 was demonstrated to be required for the maintenance of the tumorigenic phenotype in Grm1-mouse melanocytes, my project is to determine whether this is true for an epithelial cell system. With the use of Grm1-transformed mouse kidney epithelial cells, an inducible tetracycline siRNA system was introduced into the cells and tested with/without the inducer, doxycycline, for the suppression of Grm1 expression levels in vitro and in vivo. The in vivo data demonstrated decreased tumor volumes in the doxycycline treatment groups, validating the decreased expression of Grm1 seen in vitro, compared to the no treatment groups. These results provide evidence that Grm1 expression is necessary to maintain the tumorigenic phenotype of Grm1 transformed cells.
PhysicalDescription
Form
(authority = gmd)
electronic resource
Extent
vii, 53 p. : ill.
InternetMediaType
application/pdf
InternetMediaType
text/xml
Note
(type = degree)
M.S.
Note
(type = bibliography)
Includes bibliographical references (p. 46-53)
Note
(type = statement of responsibility)
by Barbara J. Wilimczyk
Name
(ID = NAME-1);
(type = personal)
NamePart
(type = family)
Wilimczyk
NamePart
(type = given)
Barbara J.
Role
RoleTerm
(authority = RULIB);
(type = )
author
DisplayForm
Barbara J. Wilimczyk
Name
(ID = NAME-2);
(type = personal)
NamePart
(type = family)
Chen
NamePart
(type = given)
Suzie
Role
RoleTerm
(authority = RULIB);
(type = )
chair
Affiliation
Advisory Committee
DisplayForm
Suzie Chen
Name
(ID = NAME-3);
(type = personal)
NamePart
(type = family)
Ganesan
NamePart
(type = given)
Shirdar
Role
RoleTerm
(authority = RULIB);
(type = )
internal member
Affiliation
Advisory Committee
DisplayForm
Shirdar Ganesan
Name
(ID = NAME-4);
(type = personal)
NamePart
(type = family)
Axelrod
NamePart
(type = given)
David
Role
RoleTerm
(authority = RULIB);
(type = )
internal member
Affiliation
Advisory Committee
DisplayForm
David Axelrod
Name
(ID = NAME-1);
(type = corporate)
NamePart
Rutgers University
Role
RoleTerm
(authority = RULIB);
(type = )
degree grantor
Name
(ID = NAME-2);
(type = corporate)
NamePart
Graduate School - New Brunswick
Role
RoleTerm
(authority = RULIB);
(type = )
school
OriginInfo
DateCreated
(point = );
(qualifier = exact)
2009
DateOther
(qualifier = exact);
(type = degree)
2009-05
Place
PlaceTerm
(type = code)
xx
RelatedItem
(type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
RelatedItem
(type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier
(type = local)
rucore19991600001
Location
PhysicalLocation
(authority = marcorg);
(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier
(type = doi)
doi:10.7282/T3VD6ZPT
Genre
(authority = ExL-Esploro)
ETD graduate
Back to the top
Rights
RightsDeclaration
(AUTHORITY = GS);
(ID = rulibRdec0006)
The author owns the copyright to this work.
Copyright
Status
Copyright protected
Availability
Status
Open
RightsEvent
(AUTHORITY = rulib);
(ID = 1)
Type
Permission or license
Detail
Non-exclusive ETD license
AssociatedObject
(AUTHORITY = rulib);
(ID = 1)
Type
License
Name
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.
Back to the top
Technical
ContentModel
ETD
MimeType
(TYPE = file)
application/pdf
MimeType
(TYPE = container)
application/x-tar
FileSize
(UNIT = bytes)
1576960
Checksum
(METHOD = SHA1)
14206a2d0905190155882e260b9fdd2fcd1b0f03
Back to the top
Statistical Profile