Somatostatin Inhibited the EMT of Pancreatic Cancer Cells by Mediating the TGF-β/Smad Signaling Pathway

Background: Pancreatic cancer (PC), a commonly recognized malignancy, arises within the digestive tract. Somatostatin (SOM) is a regulatory peptide that acts on secretion in vivo. Several studies have shown that SOM has inhibitory effects on various cancers. This work aims to probe the inhibitory effect, and mechanism of SOM action, on the epithelial-mesenchymal transition (EMT) of PC cells.Methods: First, the effects of SOM and transforming growth factor-beta (TGF-beta) on the proliferation of PC cells was determined by Cell Counting Kit-8 (CCK-8) assay. Next, we assessed the impact of SOM and TGF-beta on the metastasis and apoptosis of PC cells using transwell assays and flow cytometry. Finally, we evaluated the effects of SOM and TGF-beta on the expression of EMT-related proteins, apoptosis-related proteins, and proteins related to the TGF-beta/Smad signaling pathway in PC cells using western blot analysis.Results: SOM suppressed the growth and metastasis of PC cells, and facilitated their apoptosis (p < 0.05). Moreover, SOM reversed pro-apoptotic effects of TGF-beta (p < 0.05). Specifically, SOM increased the expression of Cysteine-aspartic acid protease 3 (Caspase-3) and Bcl-2-associated X protein (Bax) proteins while reducing the expression of B-cell lymphoma 2 (Bcl-2) protein (p < 0.05). SOM also reversed the TGF-beta-induced EMT process. The TGF-beta 1, Smad2, and Smad3 proteins in PC cells treated with SOM were significantly down-regulated (p < 0.05).Conclusions: SOM suppressed the EMT progression in PC cells through its regulation of the TGF-beta/Smad signaling pathway.