Browsing by Author "Celik, Ibrahim Seyfettin"

Filter results by typing the first few letters
Now showing 1 - 3 of 3
  • Thumbnail Image
    Article
    Metformin Induces Mitochondria-Mediated and Endoplasmic Reticulum Stress-Mediated Apoptosis and Inhibits Angiogenesis-Related Gene Expression in Breast Cancer Cells Via Targeting VEGF-A/VEGFR2/NRP1
    (Medicinska Naklada, 2025) Alizade, Ares; Evyapan, Gulsah; Celik, Ibrahim Seyfettin; Ozdem, Berna
    Aim To investigate the apoptotic and anti-angiogenic effects of metformin in human MCF7 breast cancer cells. Methods The effect of metformin on cell viability was assessed by MTS and crystal violet assays, and its effect on cell migration was evaluated by the wound healing assay. The gene expression and protein levels of angiogenesisand apoptosis-related genes were determined by realtime polymerase chain reaction, Western blot, and flow cytometry. Results Metformin reduced the viability and migration of breast cancer cells compared with the control group. Furthermore, metformin (10 mu M) increased the apoptosis-related gene and protein expression of caspase-3, Bax, AIF, CHOP and GRP78 48 hours after treatment compared with the control group. In contrast, it significantly decreased Bcl-2 and Wee1 gene and protein expression and suppressed angiogenesis-related genes VEGFA, VEGFR2, and NRP1. Conclusions Our results suggest that metformin treatment activates apoptosis pathways and inactivates the angiogenesis pathway. Although this study was conducted in vitro and did not directly evaluate blood vessel formation, the observed downregulation of angiogenesis-related genes suggests potential anti-angiogenic activity of metformin at the gene expression level.
  • Thumbnail Image
    Article
    Ornidazole Inhibits the Angiogenesis and Migration Abilities of Non-Small Cell Lung
    (Humana Press inc, 2024) Evyapan, Gulsah; Senturk, Nesrin Cetinel; Celik, Ibrahim Seyfettin
    Background: Around the world, non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths among all cancers. Despite advancements in new therapeutic approaches over the past few decades, the five-year survival rate still remains disappointing. The lack of effective anti-angiogenic and anti-migration drugs is the biggest obstacle to the treatment of metastatic lung cancer. Therefore, there is a need to develop new and effective therapeutic compounds targeting anti-angiogenic and anti-migration pathways for the treatment of lung cancer. Ornidazole is a nitroimidazole agent widely used in the treatment of parasitic infections such as trichomonas vaginalis, amebiasis and giardiasis. This study aimed to investigate the anti-proliferative, anti-angiogenic and anti-mitotic activities of the anti-parasitic drug Ornidazole in two human lung cancer cell lines (A549, H1299). Methods: We determined the effects of Ornidazole, on cell viability, apoptosis, migration, angiogenesis and metastatic ability against NSCLC in lung cancer cell lines. Its action on the mRNA and protein expression levels of VEGFA, VEGFR2, NRP1, Casp9, Casp3, Bax, Bcl-2, PIK3CA, AKT, MTOR, PTEN and FOX3A was assessed. Furthermore, in this study the effects on cell migration, cell viability and proliferation was evaluated through wound healing, MTT and Crystal violet assays. Results: This study demonstrated that Ornidazole effectively reduces cell viability and migration ability, inhibits angiogenesis and metastatic abilities in NSCLC cells. Conclusions: In conclusion, these results may shed light on the treatment of NSCLC, and we suggest the anti-parasitic drug Ornidazole as a new agent with potential anti-angiogenic and anti-mitotic activity by interfering with the molecular pathways that trigger tumor angiogenesis and migration.
  • Thumbnail Image
    Correction