MiR-26a performs converse roles in proliferation and metastasis of different gastric cancer cells via regulating of PTEN expression.

Gastric cancer is the second leading cause of cancer-related death in the world. The exact molecular pathways in gastric cancer need for further study. We herein indicated miR-26a performed converse roles on oncogenicity in different gastric cancer cells. In gastric cancer cells MKN-28, miR-26a promoted cell proliferation, migration and invasion. However, in gastric cancer cells AGS, miR-26a reduced cell proliferation and metastasis. PTEN was identified as a direct target of miR-26a. In MKN-28 cells, PTEN was suppressed by miR-26a through 3'-UTR, and PTEN mediated miR-26a promoting oncogenicity including cell proliferation and metastasis. On the other hand, in AGS cells, the expression of PTEN was enhanced by miR-26a, and PTEN mediated miR-26a reducing oncogenicity. The mechanism in AGS cells may be the indirect regulation of PTEN by miR-26a overcame the direct targeting regulation. The model like MKN-28 cells was concordant with patients with a high level of miR-26a and a low level of PTEN and patients with a low level of miR-26a and a high level of PTEN which showed lower overall survival (OS); the model like AGS cells was concordant with patients with both high level of miR-26a and PTEN and both low level of miR-26a and PTEN which showed higher OS. These findings will facilitate a better understanding of the functions and mechanisms about miR-26a, miR-26a and PTEN are potential combined biomarkers in patients with gastric cancer.