Аннотация
Hypoxia is a defining feature of the tumor microenvironment and a key driver of malignant progression through transcriptional reprogramming of metabolic, angiogenic, and survival pathways. In this study, hypoxia-induced molecular responses were investigated in human hepatocellular carcinoma (HepG2) and breast adenocarcinoma (MCF-7) cells using cobalt(II) chloride (CoCl2) as a hypoxia mimetic. Cell viability profiling was performed to determine the optimal experimental concentration, followed by quantitative PCR analysis of hypoxia-related genes and miRNA-gene interaction network analysis. Cell viability profiling identified 100 µM CoCl2 as the optimal condition for downstream analyses. Quantitative PCR revealed robust induction of HIF-1α in both cell lines, indicating activation of hypoxic signaling. However, downstream responses differed markedly between cell types. MCF-7 cells exhibited significant upregulation of SLC2A1 and increased VEGFA and NFKB1 expression, consistent with activation of glycolytic and pro-angiogenic pathways. In contrast, HepG2 cells showed limited downstream transcriptional engagement despite elevated HIF1A expression. Furthermore, miRNA-gene interaction analysis revealed a dense regulatory network in MCF-7 cells, whereas HepG2 cells displayed a more restricted, VEGFA-centered miRNA profile. These findings demonstrate that chemical hypoxia induces cell-type-specific transcriptional and post-transcriptional responses in breast and liver cancer cells. The results suggest that miRNA-mediated regulation may contribute to differential tumor adaptation to hypoxic stress and highlight the importance of cellular context in hypoxia-associated signaling pathways.