The role of IgCAM in cancer cell adhesion and migration
Bengs, Sara (2022)
Tässä tietueessa ei ole tiedostoja, ainoastaan metadata.
Bengs, Sara
2022
All rights reserved. This publication is copyrighted. You may download, display and print it for Your own personal use. Commercial use is prohibited.
Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi-fe2022022120326
https://urn.fi/URN:NBN:fi-fe2022022120326
Tiivistelmä
Cell adhesion and migration are fundamental for the normal development of multicellular organisms. An aberrant cell adhesion and migration is considered a hallmark of the metastatic cascade in cancer progression. Metastasis is the leading cause of cancer-related deaths and, thus, the early detection of tumors and the characterization of tumor invasiveness are key to increase patient survival. IgCAM is a member of the immunoglobulin superfamily (IgSF) of cell adhesion molecules (CAMs), which has been identified to be expressed in metastatic tumor cells, but not in their isogenic non-invasive counterparts. A CRISPR-Cas9 knock-out (KO) mouse model for IgCAM showed developmental defects in both the brain and intestine. Together these results suggest an important role of IgCAM in both development and cancer progression.
In this master’s thesis, the IgCAM expression levels were screened in cell lines of different cancer types. IgCAM was overexpressed in the gastrointestinal (GI) tract tumor cell line COLO320DM and the IgCAM was downregulated in the GI tract tumor cell line HT29. The IgCAM expression in these cell lines was shown using fluorescent imaging and mRNA quantification. Cell adhesion experiments on these newly generated cell lines showed that IgCAM overexpression increased cell adhesion, while downregulation of IgCAM caused loss of adhesion. Cell viability experiments showed that IgCAM downregulation resulted in decreased cell viability. Modified IgCAM expression also led to changes in the expression of genes associated with cell adhesion. These results show that IgCAM has a role in both cancer cell adhesion and viability.
Future studies aim at determining the role of IgCAM in cell migration and the metastatic cascade of cancer progression, showing if IgCAM has the potential of becoming a cancer biomarker or a target for cancer treatment.
In this master’s thesis, the IgCAM expression levels were screened in cell lines of different cancer types. IgCAM was overexpressed in the gastrointestinal (GI) tract tumor cell line COLO320DM and the IgCAM was downregulated in the GI tract tumor cell line HT29. The IgCAM expression in these cell lines was shown using fluorescent imaging and mRNA quantification. Cell adhesion experiments on these newly generated cell lines showed that IgCAM overexpression increased cell adhesion, while downregulation of IgCAM caused loss of adhesion. Cell viability experiments showed that IgCAM downregulation resulted in decreased cell viability. Modified IgCAM expression also led to changes in the expression of genes associated with cell adhesion. These results show that IgCAM has a role in both cancer cell adhesion and viability.
Future studies aim at determining the role of IgCAM in cell migration and the metastatic cascade of cancer progression, showing if IgCAM has the potential of becoming a cancer biomarker or a target for cancer treatment.