WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7150
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Article Design, Synthesis, and Evaluation of Anticancer Activities of 1,2-Diborolane Derivatives for Hepatocellular Carcinoma: an in Vitro and in Silico Study(Elsevier, 2026) Sahin, Yuksel; Antika, Gizem; Aktan, Cagdas; Metin, Kubilay; Ozgener, HuseyinHepatocellular carcinoma (HCC) is the most prevalent form of primary liver cancer and remains a major global health challenge due to limited treatment options and poor prognosis. Boron-containing compounds have garnered attention for their diverse biological activities, including pro-apoptotic effects in various types of cancer. In this study, we synthesized a panel of novel 1,2-N-substituted-1,2-diborolane derivatives and evaluated their antiproliferative, antimigratory, and apoptotic effects on hepatocellular carcinoma cell lines, HepG2 and Hep3B. Spectroscopic analyses confirmed the structural integrity of the synthesized compounds, revealing characteristic 1H-, 11B-, and 13C-NMR shifts consistent with boron-oxygen and boron-nitrogen bonding patterns. The derivatives, particularly compounds 2, 3, and 6, demonstrated potent and selective cytotoxicity toward HCC cells, with compound 3 exhibiting the lowest IC50 value (6.75 mu M) in HepG2 cells. Their time-dependent anti-proliferative effects were further supported by colony formation assays demonstrating long-term growth suppression, while wound healing assays revealed marked inhibition of HepG2 cell migration, indicating the compound's anti-metastatic potential. Our results demonstrate that the compound significantly induces apoptosis, modulates the expression of key apoptotic genes (Bax, Bcl-2, and caspase-3). In silico molecular docking further confirmed strong binding affinity to the anti-apoptotic Bcl-2 protein, supporting the proposed mechanism of action. These findings highlight the compound as a promising candidate for further preclinical evaluation in liver cancer therapy.Article Citation - WoS: 44Hesperidin Promotes Programmed Cell Death by Downregulation of Nongenomic Estrogen Receptor Signalling Pathway in Endometrial Cancer Cells(Elsevier Ltd., 2018) Cincin, Zeynep Birsu; Kıran, Bayram; Baran, Yusuf; Çakmakoğlu, BediaEndometrial carcinoma (EC) is the most common malignant gynecologic tumor in women. EC is thought to be caused by increasing estrogen levels relative to progesterone in the body. Hesperidin (Hsd), a biologically active flavonoid, could be extracted from Citrus species. It has been recently shown that Hsd could exert anticarcinogenic properties in different cancer types. However, the effects of Hsd and its molecular mechanisms on EC remain unclear. In this study, the antiproliferative, apoptotic and genomic effects of Hsd in EC and its underlying mechanisms were identified. We found that Hsd significantly suppressed the proliferation of EC cells in dose and time dependent manner. Mechanistic studies showed that Hsd could contribute apoptosis by inducing externalization of phosphatidyl serine (PS), caspase-3 activity and loss of mitochondrial membrane (MMP). Furthermore, we examined that Hsd could also significantly upregulate the expression of proapoptotic Bax subgroup genes (Bax and Bik) while downregulating the anti-apoptotic protein Bcl-2 in EC cell lines. According to GO enrichment and KEGG pathway analysis of differentially expressed genes in Hsd treated EC cells, we identified that Hsd could promote cell death via downregulation of estrogen receptor I (ESRI) that was directly related to ERK/MAPK pathway. Taken together, our study first showed that Hsd could be an antiestrogenic compound that could modulate nongenomic estrogen receptor signaling through inhibition of EC cell growth. Our findings may provide us a novel growth inhibitory agent for EC treatment after verifying its molecular mechanism with in vivo studies.