<p>Breast cancer is the most common cancer among women, with
effective treatments if the disease stays local. However, if the tumor
metastasizes, patient outcomes are significantly reduced. Mesenchymal stem
cells (MSC) have been shown to enhance metastasis by facilitating invasion and
tumor outgrowth. MCF10A Ca1h cells, a mesenchymal-like cell line, have been
shown to promote metastasis in a murine model and enhance the survival and
proliferation of their epithelial counterpart (Ca1a) in coculture. We have
established the presence of the classic MSC markers, CD90, CD105, and CD73, on
the Ca1h cells and observe a decrease in the CD90<sup>+</sup> population in the
Ca1a and fibronectin knockdown Ca1h cells. To examine the effects of this
decreased expression, a CD90 knockdown of Ca1h cells was created using
lenti-viral transduction. A decrease in fibronectin levels was seen in the CD90
knockdowns, along with a change in morphological characteristics of the cells.
To investigate the influence of a 3D microenvironment on cell phenotype, they
were also cultured on fibronectin coated scaffolds and evaluated for CD44/CD24
expression. Lastly, the knockdowns were cocultured with the Ca1a cells in a 3D
hydrogel to assess the impact of coculture on survival and proliferation. We
found that the CD90 knockdowns take on epithelial-like characteristics and
decrease survival of Ca1a cells in coculture. These findings suggest that CD90
is necessary to maintain a mesenchymal phenotype and could be used as a target
for therapies to prevent metastasis. </p>
Identifer | oai:union.ndltd.org:purdue.edu/oai:figshare.com:article/12733556 |
Date | 29 July 2020 |
Creators | Monica Chanda (9182417) |
Source Sets | Purdue University |
Detected Language | English |
Type | Text, Thesis |
Rights | CC BY 4.0 |
Relation | https://figshare.com/articles/thesis/The_Role_of_CD90_in_Breast_Cancer_Tumor_Progression/12733556 |
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