The most common kind of endometrial cancer is endometrioid endometrial cancer (EEC). SPTBN2 was shown to be highly overexpressed in EEC tissues, according to the findings. SPTBN2 overexpression was linked to a poor prognosis.
Furthermore, researchers demonstrated that knocking down SPTBN2 dramatically reduced EEC cell proliferation, migration, and invasion. SPTBN2 might also interact with CLDN4 to increase endometrial cancer metastasis via the PI3K/AKT pathway, according to the findings. They then showed that CLDN4 is increased in EEC and promotes metastasis. CLDN4 overexpression may have partially corrected the reduction in cell migration and invasion induced by SPTBN2 deficiency. Furthermore, they discovered that SPTBN2 is a target of miR-424-5p, a tumor suppressor in endometrial cancer. SPTBN2 inhibition partly reversed the impact of miR-424-5p in EEC, according to rescue trials.
Finally, they showed that SPTBN2 might interact with CLDN4 to increase endometrial cancer metastasis via the PI3K/AKT pathway in EEC by functioning as a prominent target of miR-424-5p. SPTBN2 was found to have prognostic and metastatic effects in EEC, indicating that it might be used as a prognostic biomarker as well as a target for metastasis treatment.