MIF has been shown to promote tumor immune escape mechanisms in other cancer entities, which makes it an interesting target for cancer therapy, given the known significance of immune mechanisms for uterine cervical cancer. The overexpression of MIF on the protein and mRNA level, as well as its secretion by cervical cancer cells points to a critical role of the protein for the pathogenesis of uterine cervical cancer.
Galectin-1, a member of the beta-galactoside-binding family, is widely expressed in epithelial and immune cells. It is involved in several normal and pathologic processes, such as cancer progression, metastasis, and immunobiology. Galectin-1 was found to be overexpressed in various cancer cells and the corresponding benign tissue. Therefore, it has been described as a marker for tumor progression in some malignancies. In the current study, the expression of galectin-1 was examined in 80 formalin-fixed, paraffin-embedded cervical tissues: 20 benign cervical specimen, 20 low-grade squamous intraepithelial lesions (LGSIL), 20 high-grade squamous intraepithelial lesions (HGSIL), and 20 invasive squamous cell carcinomas (ISCC). Immunohistochemical analyses showed that the intensity of the galectin-1 expression on stromal cells next to the transformed cells increased according to the pathologic grade: benign cervical tissue < LGSIL < HGSIL < ISCC (P < 0.001). The epithelial cells were always negative for galectin-1. These results suggest that galectin-1 expression on stromal cells increases with the histopathologic grade of cervical tissues, and it can be concluded that this increase is associated with the progression of cervical neoplasia.
The results suggest that both TKTL1 and p-Akt play an important role in the progression of cervical neoplasia, which may be due to their impact on glycolysis.
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