The complement system is a key component of the innate immune response and plays a dual role in cancer, as it can participate in the elimination of cancer cells or promote their survival and growth. One of the main membrane-bound complement regulators is CD55, also known as decay-accelerating factor (DAF), which inhibits complement activation by accelerating the decay of C3 and C5 convertases, thereby preventing the formation of the membrane attack complex. Increased CD55 expression is often associated with more aggressive forms of cancer and with mechanisms of immune evasion. In this thesis, we aimed to compare CD55 expression among different human cancer cell lines originating from various tissue types. We cultured the selected cell lines and prepared cell lysates from them. Protein separation was performed using SDS-PAGE electrophoresis, followed by Western blot transfer and the use of specific anti-CD55 antibodies to assess the presence and expression of this protein. CD55 was detected only in the MDA-MB-231 (triple-negative breast cancer) cell line, whereas no signal was observed in HepG2 (liver cancer), A549 (lung cancer), and MCF7 (breast cancer) cell lines. This is consistent with literature describing high basal CD55 expression in aggressive and metastatic cell lines, and lower expression in less aggressive cell lines. Our findings confirm that CD55 expression is highly dependent on the cell line and its phenotype, and further support the investigation of CD55 as a potential biomarker and therapeutic target in the treatment of aggressive tumors.
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