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ABSTRACTS – Contributed Posters
inhibited cell proliferation of both SCC1 and SCC23 cells.
Cell cycle analysis showed that the inhibitors affected cell
cycle progression of both SCC1 and SCC23 similarly in
that the percentage of cells in S and G2 phase increased at
the expense of those in G1. Conclusion: Based on our data,
JMJD2 inhibitors A70 and SD70 can effectively inhibit SCC
proliferation and can possibly be a target for the treatment of
head and neck cancers.
165 Role of IL-6 Family Cytokines in Breast Tumor Cell
Expression of VEGF, MADHURI NANDAKUMAR*,
DANIELLE HEDEEN and CHERYL JORCYK
(Department of Biological Sciences, Boise State
University, 1910 University Drive, Boise, ID-8372;
madhurinandakumar@u.boisestate.edu).
OSM is a multifunctional IL-6 family cytokine produced
by many cells including human T-Lymphocytes, neutrophils,
macrophages and monocytes. Studies from our lab and others
provide evidence that OSM plays an important role in tumor
progression through stimulation of detachment, invasion invitro
and induction of the pro-angiogenic factor, vascular
endothelial growth factor (VEGF). Our current studies were
designed to determine differential secretion of VEGF in
breast cancer cells induced by IL-6 family cytokines. Our
results indicate an increased secretion of OSM-induced
VEGF. Effect of these inflammatory cytokines on endothelial
tube formation and neo-vascularisation, in vivo, were also
measured. Our results also provide insight into the effects of
inflammatory cytokines on inducing important transcription
factors. These results may provide important insight into
understanding signaling pathways involved in cytokinemediated
VEGF induction.
Funded by NIH R15CA137510, ACS RSG-09-276-01-CSM, Susan G
Komen for the cure KG100513, and NIH/NCRR P20RR016454.
166 Parathyroid Hormone Related Protein (PTHrP)
Regulates Expression Of Estrogen Receptor In Bone And
Breast, KELSEY BRUCH, HANNAH DYAR* and
MINOTI HIREMATH (Department of Biological Sciences,
Boise State University, 1910 University Drive, MS1515,
Boise, ID 83725; Hannah.dyar@gmail.com, kelseybruch@u.
boisestate.edu and minotihiremath@boisestate.edu).
Parathyroid Hormone Related Protein Protein (PTHrP)
acts as a local cell-signaling factor to regulate mammary
development in the embryo. PTHrP is required for formation
of the mammary mesenchyme, which is a collection of
stromal cells that condensed around the invading epithelial
component of the mammary gland. Mammary mesenchymal
cells express specific proteins including estrogen receptor
(ER). ER expression is abolished in PTHrP -/- mice and
is expanded to the ventral dermis by overexpression of
PTHrP. To determine if PTHrP regulates ER expression
in other systems, we harvested RNA from PTHrP-treated
and untreated osteoblasts. ER expression was analyzed by
semi-quantitative PCR. Our preliminary results show that
PTHrP treatment results in a 2-fold increase in ER levels.
To determine if PTHrP affects ER protein, we treated
T47D and MCF7 breast cancer cells with PTHrP for 24
hours. Immunofluorescence and Western blotting indicated
that PTHrP increases ER protein expression in these cells.
Taken together, out studies suggest that PTHrP regulates
ER expression in bone and breast. Declining levels of
estrogen are implicated in the etiology of postmenopausal
osteoporosis. Our data suggests that exogenous PTHrP is a
novel potential treatment to sensitize osteoporotic bone to
declining estrogen levels by increasing the expression of
ER. Moreover, we predict that PTHrP treatment could also
be used as an adjuvant therapy to sensitize breast cancers
to Tamoxifen, an anti-estrogen currently widely used as a
treatment for breast cancer.
167 Does Oncostatin M Induce Morphological
Changes in Human Breast Cancer Cells NICOLE
ANKENBRANDT*, HUNTER COVERT, and CHERYL
JORCYK (Department of Biology, Boise State University,
1910 University Dr., Boise, ID 83725; nicoleankenbrandt@u.
boisestate.edu).
Currently in the United States, 1 in 8 women are at risk
of acquiring breast cancer in their lifetime. The interleukin-6
(IL-6) family cytokine oncostatin M (OSM) was originally
believed to reduce breast tumor cell proliferation, but recent
data suggests that OSM may promote tumor metastasis by
breaking cell-cell adhesion. Therefore, it is the research goal
of this lab to determine the mechanisms behind the disease
and to examine the effects of OSM on the morphological
changes of the human breast cancer cell lines, MCF-7 and
MCF-7 luc. One of the proposed mechanisms for tumor
metastasis utilizes the process of tumor cell detachment and
change in morphology. We hypothesize that OSM promotes
cell detachment by reducing cell-cell adhesion proteins
such as E-cadherin and α-catenin. This hypothesis will be
tested by observing morphological changes with and without
OSM and immunocytochemistry (ICC) of E-cadherin and
α-catenin along with phalloidin staining for actin. Actin
filaments provide mechanical support for cells, as well as
determine their shape, and allow for division and migration.
These studies will allow us to understand the mechanism by
which OSM leads to inhibited breast tumor cell proliferation
and yet increased metastatic potential.
168 The Effects of Chemotherapy Drugs, Paclitaxel and
Cisplatin, Combined with NAC on Pancreatic Cancer Stem
Cells, CARLOS ANAYA¹*, KATELYNN BARKLEY¹*,
Han-Ching Helen Tseng², Gabriella
Orona², and Anahid Jewett² (¹Howard Hughes
Medical Institute Pre-College Science Education Program
at UCLA; ²The Weintraub Center for Reconstructive
Biotechnology; UCLA School of Dentistry, 10833 Le Conte
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