| Summary: | 碩士 === 國防醫學院 === 微生物及免疫學研究所 === 104 === Colorectal cancer is the third most common malignancy and the fourth largest cause of cancer mortality, the reason why colorectal cancer causes such high mortality is that cancer cells may become resistance to chemotherapy and metastasize to other organs in late stage. Epithelial-Mesenchymal Transition (EMT) has been reported in many advanced cancers, and contributed to tumor progression by promoting tumor invasion, metastasis, and drug resistance. Snail is a transcription factor that mediates the EMT in several tumor types, including colorectal cancer (CRC). Overexpression of snail could induce EMT and acquire chemo resistance. In our preliminary data, overexpression of Snail in CRC cells did not affect cell viability, but significantly increased drug resistance and migration ability. However, we could not repeat these experiments because of the SNAIL-overexpressing lines are not stable. Therefore, we want to use a tet-on-inducible system and knockdown strategy to reconfirm whether Snail contributes to chemoresistance and explore the possible mechanism.
In the study, first, we have established an inducible system to overexpress Snail. Our data found that overexpression of Snail did not significantly affect EMT phenotype but increase drug resistance in HT29 cells. Next, we used shRNA to knockdown the expression of Snail. And we found that knockdown of Snail decreased drug resistance in SW620 cells. Finally, we found that neither overexpression nor knockdown of Snail can affect AKT survival signal pathway in CRC cell lines. Till now, our data found that Snail contributing to drug resistance is not through the AKT survival signaling pathway.
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