Abstract

Colorectal cancer (CRC) is a relatively common malignant tumor of the digestive system. In this research, the impact of quercetin (Que) on fecal syndecan-2 (SDC2) gene methylation levels in CRC patients and its potential mechanisms of action were analyzed. Retrospective analysis was conducted on data from 56 CRC patients admitted to our outpatient department. The methylation status of SDC2 in fecal samples and the sensitivity and specificity of fecal SDC2 gene detection were analyzed. Subsequently, MTT assay was performed to assess the impact of Que on cell viability of SW480 cells during the growth phase. The blank control consisted of 200 μL of L-15 medium, the solvent control group consisted of 200 μL of L-15 medium+150 μL of dimethyl sulfoxide (DMSO), and the experimental group consisted of 200 μL of L-15 medium+different concentrations of Que (5, 10, 20, 40, 80, 120 μmol/L). After SW480 cells were treated with various concentrations of Que, protein expression (EP) levels of C-Myc, B-cell lymphoma (Bcl)-2, phosphorylated STAT3 (p-STAT3), and interleukin (IL)-6 were determined by qRT-PCR and Western blot. The single-gene detection of SDC2 in fecal samples yielded an area under the curve (AUC) of 0.763 (95% confidence interval (CI): 0.623–0.876). As the concentration of Que increased, the OD values decreased. Various concentrations of Que exhibited varying inhibitory effects on SW480 cell proliferation (CP) at different time intervals, with the OD values at 72 h being superior to those at 48 h and 24 h. The OD values at 48 h were superior to those at 24 h, indicating a significant enhancement of SW480 proliferation with prolonged time. As the treatment concentration increased, the cell viability gradually decreased. Que at concentrations ranging from 20 to 160 μmol/L showed a notable inhibition of SW480 CP. With increasing concentrations of Que, protein levels of C-Myc, Bcl-2, p-STAT3, and IL-6 decreased gradually. In summary, Que can inhibit the EP of inflammatory factors in CRC patients, suppress tumor CP by downregulating protein levels of C-Myc, Bcl-2, p-STAT3, and IL-6, and thus exert an anti-CRC effect.

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