The Role of FGFR2 on Proliferation, Apoptosis and Glucose Metabolism of Breast Cancer Cells

The present study investigated the expression of miR-598 in both breast cancer tissues and cells. Overexpression systems were established by introducing miR-598 mimics and pcDNA- Fibroblast Growth Factor Receptor 2(FGFR2) plasmids, either individually or in combination, into breast cancer cells. Four groups were constituted for probing purposes: control group, miR-598 mimics group, pcDNA-FGFR2 group, and mimics+FGFR2 group. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to measure the expression of miR-598 and FGFR2. Furthermore, bioinformatics software was used to predict and identify the possible binding sites between miR-598 and FGFR2. To validate the predicted binding sites, a dual-luciferase reporter gene experiment was carried out. A clone formation assay was used to evaluate cell proliferation, while glucose consumption and lactic acid production assays were conducted using a kit. Moreover, Western blot analysis was done to ascertain the expression of Bcl-2, Bax, Caspase-3, and Caspase-9 proteins. The expression of miR-598 in breast cancer tissues and cell lines was found to be significantly lower than that in normal breast tissues and cell lines, respectively (P < 0.05). It was also revealed that FGFR2 is the target gene of miR-598 and there is an inverse correlation between the two. Overexpression of miR-598 led to a decrease in clonal formation rate caused by high FGFR2 levels. Moreover, the overexpression of miR-598 reversed the effects induced by high FGFR2 levels, such as increased mitochondrial membrane potential and reduced expression of apoptosis-associated proteins. The microRNA miR-598 has been found to decrease the proliferation of breast cancer cells by targeting FGFR2, inducing apoptosis, and suppressing glucose consumption.