Investigation of cytotoxic, molecular and in silico effects of chlorambucil and tamoxifen on 2D/3D MDA-MB-231 and HeLa cancer cell models.
This study aimed to investigate the cytotoxic, morphological, and molecular effects of Tamoxifen (TMX) and Chlorambucil (CHL) on breast cancer (MDA-MB-231) and cervical cancer (HeLa) cell lines. The impact of these agents on metastatic behavior, apoptotic mechanisms, and gene expression profiles was examined in both two-dimensional (2D) and three-dimensional (3D) cell culture models.
Cells were treated with varying concentrations of TMX and CHL. Cytotoxicity was assessed using the XTT assay, and morphological changes were monitored by microscopy. Migration and invasion assays assessed metastatic potential. VEGFA expression was quantified by qRT-PCR. In 3D cultures, treatment responses were evaluated based on size reduction and structural changes in hydrogel-based spheroids. Docking analysis was conducted to determine binding affinities of TMX and CHL.
TMX and CHL exhibited dose-dependent effects on breast and cervical cancer cells. Combination treatment led to significantly greater reductions in cell viability compared to controls (p < 0.05). Moreover, VEGFA expression was markedly reduced in both 2D and 3D models (p < 0.05). These findings support the potential therapeutic value of TMX and CHL. Docking analysis revealed highly negative binding energies, consistent with in vitro results, indicating synergistic interaction at molecular and cellular levels.
TMX and CHL combination therapy demonstrated potent anti-cancer activity in breast and cervical cancer models, reducing cell viability, metastatic capacity, and VEGFA expression. These results suggest that TMX and CHL, when used together, may represent a promising strategy for developing synergistic and targeted cancer therapies. Further in vivo and clinical validation is warranted.
Cells were treated with varying concentrations of TMX and CHL. Cytotoxicity was assessed using the XTT assay, and morphological changes were monitored by microscopy. Migration and invasion assays assessed metastatic potential. VEGFA expression was quantified by qRT-PCR. In 3D cultures, treatment responses were evaluated based on size reduction and structural changes in hydrogel-based spheroids. Docking analysis was conducted to determine binding affinities of TMX and CHL.
TMX and CHL exhibited dose-dependent effects on breast and cervical cancer cells. Combination treatment led to significantly greater reductions in cell viability compared to controls (p < 0.05). Moreover, VEGFA expression was markedly reduced in both 2D and 3D models (p < 0.05). These findings support the potential therapeutic value of TMX and CHL. Docking analysis revealed highly negative binding energies, consistent with in vitro results, indicating synergistic interaction at molecular and cellular levels.
TMX and CHL combination therapy demonstrated potent anti-cancer activity in breast and cervical cancer models, reducing cell viability, metastatic capacity, and VEGFA expression. These results suggest that TMX and CHL, when used together, may represent a promising strategy for developing synergistic and targeted cancer therapies. Further in vivo and clinical validation is warranted.