CHREBP suppresses gastric cancer progression via the cyclin D1-Rb-E2F1 pathway

Accumulating evidence has demonstrated that carbohydrate response element binding protein (CHREBP) has a crucial function in tumor pathology. In this study, we found CHREBP downregulation in gastric cancer (GC) tissues, and CHREBP was determined to be an independent diagnostic marker of GC. The downregulation of CHREBP promoted cell proliferation and inhibited apoptosis. Moreover, the level of cyclin D1 was significantly correlated with CHREBP expression in GC and paracancerous normal samples. In addition, CHREBP transcriptionally inhibited cyclin D1 expression in GC cells. Tumor suppressor activity of CHREBP could be affected by the upregulation of cyclin D1. In summary, CHREBP was found to be an independent diagnostic marker of GC and to influence GC growth and apoptosis via targeting the cyclin D1-Rb-E2F1 pathway.

Automated summary

Accumulating evidence suggests that downregulation of carbohydrate response element binding protein (CHREBP) is associated with gastric cancer (GC) development and progression. CHREBP acts as an independent diagnostic marker of GC and its downregulation promotes cell proliferation and inhibits apoptosis. Furthermore, CHREBP transcriptionally inhibits cyclin D1 expression in GC cells, suggesting its involvement in GC growth and apoptosis through targeting the cyclin D1-Rb-E2F1 pathway.