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An integrated study was conducted to identify the potential prognosis biomarker of the gastric cancer. The study analyzed the expression level of microRNAs (miRNAs) and clinical follow-up information of gastric cancer patients. miR-371-3p was determined as a promising biomarker for the prognosis of GCs among the 74 dysregulated miRNAs examined. The qRT-PCR analysis of the expression of miR-371-3p in 121 GC tumors confirmed its overexpression and correlation with aggravation of the GC patients. The in vitro functional assays demonstrated that overexpression of miR-371-3p promoted proliferation, colony formation, migration and invasion of the GC cells, whereas miR-371-3p depletion led to the opposite. The findings were further confirmed by the in vivo knockdown of miR-371-3p experiment: the depletion of miR-371-3p inhibited tumor growth and metastasis. Based on the results of the bioinformatics analysis and bioassays, TOB1 was found to be the direct target of miR-371-3p, functioning as a tumor suppressor in GC cells. TOB1 was prerequisite for miR-371-3p to promote cell proliferation and migration. In conclusion, the results suggest that miR-371-3p is a potential prognosis biomarker and therapeutic target for GC., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Radiotherapy has been the primary method for the local control of several types of unresectable tumor, including gastric cancer. Patients with gastric cancer frequently express high levels of epidermal growth factor receptor (EGFR), which have been found to increase following radiotherapy treatment. This provides a basis for the combination of antibodies targeting EGFR and radiotherapy. In our previous study, a protein (anti‑EGFR‑iRGD) with bispecific targets and high permeability was constructed, and its effects on inhibiting the proliferation of gastric cancer cells was investigated. In the present study, the capacity of anti‑EGFR‑iRGD to modulate a radiation response was investigated and the specific mechanisms underlying these interactions were evaluated in gastric cancer cell lines and xenografts exhibiting high levels of EGFR. The radioenhancement of anti‑EGFR‑iRGD was associated with inhibited radiation‑induced upregulation of EGFR, inhibited cell proliferation and promotion of cell apoptosis. In addition, anti‑EGFR‑iRGD appeared to permeate more into the tumor tissue following radiation. These findings indicated that the recombinant protein anti‑EGFR‑iRGD was a selective and effective radiosensitizer in EGFR‑overexpressing gastric cancer cells and xenografts. These results further suggested that anti‑EGFR‑iRGD is a potential superior EGFR‑targeted therapy combined with radiotherapy. Overall, the present study suggested that anti‑EGFR‑iRGD may be a promising candidate for preclinical and clinical use.