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Ovarian cancer (OC) is a common gynecological malignant carcinoma worldwide. Accumulating research has revealed that multiple microRNAs (miRNAs) are abnormally expressed at different levels in various malignancies, playing vital roles in tumorigenesis. This study investigated the regulatory functions and potential mechanism of miR-126 in OC proliferation, invasion and migration. It was found that miR-126 was prominently downregulated in OC. Moreover, the decrease of miR-126 promoted the aggressive phenotypes and indicated poor prognosis of OC patients. Functional assays demonstrated that restoration of miR-126 dramatically repressed OC cell proliferation, migration and invasion. Furthermore, luciferase reporter assay was conducted to verify putative binding sites of miR-126 in the epidermal growth factor-like domain 7 (EGFL7) 3 untranslated region (3′UTR), indicating that EGFL7 was a target gene of miR-126 in OC cells. It was further discovered that miR-126 exerts its function on regulating ERK/MAPK pathway and epithelial-to-mesenchymal transition (EMT) in OC cells. The above findings suggested that miR-126 served as a cancer suppressor in OC, suggesting a promising application of miR-126 in the clinical diagnosis and therapeutics of OC.

MicroRNAs (miRs) have been demonstrated to be associated with the development, progression and prognosis of gastric cancer. However, the exact role of miR‑27b in the regulation of gastric cancer cells and the underlying mechanisms remain unclear. In the current study, it was demonstrated that miR‑27b was significantly upregulated in gastric cancer tissues and cell lines, compared with their matched normal adjacent tissues and normal gastric epithelial cells, respectively. Luciferase reporter assay data indicated that sprouty2 (SPRY2) is a direct target of miR‑27b, and miR‑27b binds to the 3'‑untranslated region of SPRY2 mRNA. Overexpression of miR‑27b led to a significant reduction in the protein expression of SPRY2, while knockdown of miR‑27b enhanced the SPRY2 protein expression in gastric cancer cells. Furthermore, knockdown of miR‑27b promoted migration and invasion in gastric cancer cells, exhibiting similar effects to those of SPRY2 overexpression on the migration and invasion of gastric cancer cells. Investigation of the molecular mechanisms identified that the activity of extracellular signal‑related kinase (ERK) signaling was mediated by miR‑27b and SPRY2 in gastric cancer cells. In addition, it was observed that SPRY2 was frequently downregulated in gastric cancer tissues compared with their matched normal adjacent tissues. In summary, it was suggested that miR‑27b promotes the migration and invasion of gastric cancer cells via inhibition of SPRY2‑mediated ERK signaling. Therefore, miR‑27b/SPRY2 may be used as a potential target for the treatment of gastric cancer.