In this doctoral thesis we investigated the role of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) in colorectal cancer (CRC) progression and metastasis.
Firstly, we showed that EMT and MET play an important role in the progression and metastasis of CRC, but not as full EMT/MET, but as partial EMT/MET. We demonstrated that EMT and MET are involved in both lymphogenic and hematogenous tumor spread. Additionaly, we showed that EMT markers at the invasive front of advanced CRC cannot serve as additional predictive factors of metastasis.
Secondly, we demonstrated that partial EMT is activated at the invasive front of CRC exhibiting an infiltrative growth, where tumor budding and/or poorly differentiated clusters are present, while EMT is not activated at the invasive front exhibiting an expansive growth.
Thirdly, we demonstrated that punching tissue block is a adequate technique for studying the differences in tumor gene expression between the central part and the invasive front of CRC, but is insufficient to analyze and compare morphologically distinct patterns along the invasive front, including tumor budding. For this purpose, the use of laser capture microdissecton is essential.
Lastly, we used bioinformatics analysis to identify long non-coding RNAs that could be involved in regulation of EMT in CRC.
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