Gastric cancer (GC) is the third most common cause of cancer-associated mortality in China. Aberrant microRNA (miR) expression can occur through multiple biological processes and has been implicated in cancer development. However, to the best of our knowledge, the function of miR-502-5p in GC is currently unclear. In the present study, the expression and function of miR-502-5p in GC was evaluated. Reverse transcription-quantitative (RT-q) PCR was used to measure the expression levels of miR-502-5p in GC tissues, normal adjacent tissues, a normal human gastric epithelial cell line (GES-1) and two GC cell lines. miR-502-5p expression levels were significantly lower in GC tissues and GC cell lines compared with those in adjacent normal tissues and GES-1 cells, respectively. Subsequently, the target genes of miR-502-5p were predicted, and it was demonstrated that the transcription factor SP1 was a direct target. SP1 expression, cell viability, migration and invasion, and SP1 protein levels were examined using RT-qPCR, an MTT assay, Transwell assay and western blotting, respectively. Human GC cells were then transfected with an miR-502-5p mimic to emulate miR-502-5p overexpression, resulting in inhibition of the proliferation, migration and invasion capacities of human GC cells. Compared with the negative control, cells overexpressing miR-502-5p had decreased levels of SP1 mRNA and protein. These data suggest that miR-502-5p serves as a tumor suppressor gene by targeting SP1 to regulate the proliferation, migration and invasion of GC cells.

Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)-224-5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription-quantitative PCR was used to explorethe expression of miR-224-5p and the PTEN gene. MTT, wound healing, Transwell and tumorigenesis assays were conducted to investigate the proliferation, migration and invasion of MCC1 cells in vitro and in vivo. Western blot analysis was employed to test the protein expression of PTEN. The target gene of miR-224-5p was assessed and verified by luciferase assay. miR-224-5p expression was notably higher, while PTEN expression was lower, in MCC1 cells compared with normal tissues and cells. Overexpression of miR-224-5p promoted the proliferation, migration and invasion of MCC and knockdown of miR-224-5p inhibited these functions. Bioinformatics analysis and luciferase assay indicated that PTEN was the direct target gene of miR-224-5p. The negative correlation between miR-224-5p and PTEN was confirmed both in vitro and in vivo. PTEN reversed the effects of miR-224-5p on proliferation, migration and invasion of MCC1 cells. The present study revealed for the first time, to the best of the authors' knowledge, that miR-224-5p was highly expressed and served an oncogenic role in MCC. miR-224-5p not only regulated the proliferation, migration and invasion of pancreatic MCC but may also be a potential therapeutic target for MCC.

The prognosis of invasive pancreatic mucinous cystadenocarcinoma (MCC) is poor, and the molecular mechanism underlying its development remains unclear. The present study aimed to explore the potential role of autophagy in pancreatic MCC. The results demonstrated an increase in autophagy signaling in pancreatic MCC tissues and the MCC1 cell line compared with adjacent tissues and normal human pancreatic ductal epithelium (HPDE) cells. In addition, abnormal autophagy activation facilitated the migration and invasion of MCC1 cells. MicroRNA (miR)-224-5p expression levels were significantly higher in MCC1 cells compared with those in HPDE cells. Treatment with rapamycin further demonstrated that high levels of autophagy elevated miR-224-5p expression in MCC1 cells in a time-dependent manner. BCL2 was identified as a downstream target gene of miR-224-5p, which binds to the 3'-untranslated region of BCL2. In addition, the results of the present study demonstrated that BCL2 knockdown reversed the inhibition of autophagy mediated by the miR-224-5p inhibitor. To the best of our knowledge, this is the first study to evaluate the role of autophagy in pancreatic MCC. Thus, these results suggested that autophagy may be hyperactivated in pancreatic MCC. In addition, the present study identified a positive feedback loop between autophagy signaling and miR-224-5p, which may promote the aggressive migration and invasion of MCC1. These results may provide a new insight into the relationship between autophagy and tumor metastasis in pancreatic MCC.