MiR-590 Targets SHP2 to Promote Cervical Cancer Proliferation and Tumor Formation through Regulation of the JAK-STAT Signaling Pathway

Objective To investigate the mechanism by miRNA-590 targets SHP2 to regulate the JAK-STAT signaling pathway, thereby promoting cell proliferation and tumor formation in cervical cancer. Methods Immunohistochemistry was employed to assess the expression levels of SHP2 and JAK1 in cervical cancer tissues and analyze their correlation with clinical pathological features. RNA interference and overexpression techniques were used to silence and overexpress SHP2, respectively, to evaluate its impact on cell proliferation, migration, and apoptosis in cervical cancer cells. Western blot and qPCR were utilized to examine the regulatory effect of SHP2 on the JAK-STAT signaling pathway. Further, the effect of miR-590 overexpression on cervical cancer cell proliferation, migration, and JAK-STAT signaling was investigated. Results Immunohistochemical analysis revealed that SHP2 and JAK1 were significantly upregulated in cervical cancer tissues, and high expression of SHP2 was strongly correlated with tumor stage and size. Cell experiments showed that overexpression of SHP2 significantly promoted cell proliferation and migration while inhibiting apoptosis, whereas SHP2 silencing suppressed these behaviors and promoted apoptosis. Western blot and qPCR analyses further confirmed that SHP2 activated the JAK1-STAT3 signaling pathway to enhance cell survival and migration. Animal model experiments supported the findings of the cell-based assays. Additionally, miR-590 was found to directly target SHP2, downregulating its expression and significantly inhibiting cervical cancer cell proliferation and migration. Conclusion SHP2 promotes cell proliferation, migration, and apoptosis resistance in cervical cancer by activating the JAK-STAT signaling pathway. miR-590 exerts its anti-cancer effects by downregulating SHP2 expression, providing a potential therapeutic strategy for cervical cancer.