Background: Gastrin (GAST)  is a well-known hormone regulating gastric biofunctions in the secretion of acid and maintaining its structural integrity. Furthermore, the dysregulation of GAST  is also involved in the development of various forms of cancer. However, there are some limitations for illustrating the cellular regulation of GAST  and its regulatory mechanisms in gastric malignant transformation and the potential epigenetic regulators systematically.
Methods: We explored the role of GAST  expression in gastric cancer (GC) and normal tissues with the clinical features and investigated the potential relationship between GAST  and STAT3/MMP11  pathway by gain or loss of function analyses. Besides, based on our microRNA/mRNA expression profiles, miR-30a-3p  was the potential epigenetic regulator and additional experiments were performed to identify the hypothesis.
Results: Elevated GAST  expression was frequently detected in GC and was associated with worse outcomes (p< 0.001). And we firstly demonstrated that GAST  was negatively regulated by miR-30a-3p . Moreover, GAST  induced GC cell proliferation, migration and invasion mediating STAT3/MMP11  pathway in this study.
Conclusion: MiR-30a-3p  was the promising suppressor gene through negatively regulating the expression of GAST , and dysregulation of GAST  was a prognostic signature associated cell proliferation and metastasis through STAT3/MMP11  pathway in GC.
Keywords: gastrin , proliferation, invasion, miR-30a-3p , STAT3/MMP11 pathway, gastric cancer