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    Regulation of Nrf2/Keap1 signaling pathway in cancer drug resistance by galectin-1: cellular and molecular implications
    (Oae Publishing Inc, 2024) Yaylim, Ilhan; Aru, Melek; Farooqi, Ammad Ahmad; Hakan, Mehmet Tolgahan; Buttari, Brigitta; Arese, Marzia; Saso, Luciano
    Oxidative stress is characterized by the deregulation of the redox state in the cells, which plays a role in the initiation of various types of cancers. The activity of galectin-1 (Gal -1) depends on the cell redox state and the redox state of the microenvironment. Gal -1 expression has been related to many different tumor types, as it plays important roles in several processes involved in cancer progression, such as apoptosis, cell migration, adhesion, and immune response. The erythroid-2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway is a crucial mechanism involved in both cell survival and cell defense against oxidative stress. In this review, we delve into the cellular and molecular roles played by Gal -1 in the context of oxidative stress onset in cancer cells, particularly focusing on its involvement in activating the Nrf2/Keap1 signaling pathway. The emerging evidence concerning the anti-apoptotic effect of Gal -1, together with its ability to sustain the activation of the Nrf2 pathway in counteracting oxidative stress, supports the role of Gal -1 in the promotion of tumor cells proliferation, immuno-suppression, and anti -tumor drug resistance, thus highlighting that the inhibition of Gal -1 emerges as a potential strategy for the restraint and regression of tumor progression. Overall, a deeper understanding of the multi -functionality and disease -specific expression profiling of Gal -1 will be crucial for the design and development of novel Gal -1 inhibitors as anticancer agents. Excitingly, although it is still understudied, the ever-growing knowledge of the sophisticated interplay between Gal -1 and Nrf2/Keap1 will enable researchers to gain valuable insights into the underlying causes of carcinogenesis and metastasis.
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    TRAIL C1595T Variant Critically Alters the Level of sTRAIL in Terms of Histopathological Parameters in Colorectal Cancer
    (Springer India, 2023) Horozoglu, Cem; Yildiz, Asli; Sonmez, Dilara; Demirkol, Seyda; Yildiz, Yemliha; Arikan, Soykan; Yaylim, Ilhan
    TRAIL, a member of the TNF family, is expressed in tumor and tumor surrounding tissue in many solid organ cancers. While the induction of tumor-specific apoptosis in correlation with cytokine stimulation may cause anti-tumoral effects, the pro-tumorigenic effects of its expression by tumor surrounding tissue members have been reported in the literature. In our study, it was aimed to evaluate the effect of the gene variant of TRAIL on soluble levels in patients with colorectal cancer (CRC) on the molecular pathological axis. TRAIL C1595 gene variant PCR-RFLP and sTRAIL levels were determined by ELISA in age and sex adjusted CRC and control groups. It was determined that CT carriage was high in patients without perineural invasion and sTRAIL levels were approximately 2.72 times lower than CC in patients with CT in this group (p < 0.05). Similarly, sTRAIL level was found to be high in patients with CC genotype in CRC without lymph node metastas. It was determined that CT carriage was high in patients without perineural invasion and sTRAIL levels were approximately 2.49 times lower than CC in patients with CT in this group.is (p < 0.05). We think that TRAIL C1595T in CRC can change sTRAIL levels in the clinicopathological axis in advanced stages such as metastasis and invasion, but both are not independent risk factors.