High glucose enhances malignant progression of MDA-MB-231 cells through cumulative effect.

Previous investigations have shown that high glucose can promote breast cancer progression. However, the relationship between high glucose microenvironment and triple-negative breast cancer (TNBC) remains to be explored. In this study, we performed RNA-seq to explore the effect of short-term high glucose and long-term high glucose on MDA-MB-231 cell line. A total of 896 highly ranked differentially expressed genes (DEGs) were identified, including 57 DEGs of short-term high glucose group and 839 DEGs of long-term high glucose group. The DEGs of short-term high glucose group were mainly associated with IL-17 signaling pathway. Nonetheless, the DEGs of long-term high glucose group were primarily involved in IL-17 signaling pathway, MAPK signaling pathway, TNF signaling pathway, AGE-RAGE signaling pathway in diabetic complications, Toll-like receptor signaling pathway, and VEGF signaling pathway. Additionally, 8 hub genes of short-term high glucose group were enriched in metabolic pathway. Moreover, 10 hub genes of long-term high glucose group were enriched in ribosome pathway. Subsequently, in vitro experiment results found that high glucose can promote cell proliferation, and has a time accumulation effect. In addition, high glucose can induce the accumulation of inflammatory factors and promote angiogenesis. Collectively, these findings provide novel insights into the effect of diabetes mellitus type 2 (T2DM) on TNBC. [Display omitted] • This study comprehensively analyzed the gene expression profile of MDA-MB-231 cells in a high-glucose microenvironment. • High glucose promotes proliferation and angiogenesis of MDA-MB-231 cells and induces accumulation of inflammatory factors. • High glucose can elevate the concentration of IL-17, exhibiting a time-dependent accumulation effect. • High glucose can regulate the progression of MDA-MB-231 cells by multiple approaches. [ABSTRACT FROM AUTHOR]