LAUSR

Aberrantly expressed miRNAs play a crucial role in the progression of lung adenocarcinoma. However, to date, the role of miR‑888 in lung adenocarcinoma progression is unclear. In the present study, the biological function of miR‑888 and its underlying mechanism in lung adenocarcinoma progression were explored. RT‑qPCR was performed to detect the expression of miR‑888 in 38 matched lung adenocarcinoma samples respectively. Next, the effects of miR‑888 on the proliferation, invasion and migration of lung adenocarcinoma A549 cells were evaluated by a series of gain‑ and loss‑of‑function assays. Our results revealed that miR‑888 was significantly upregulated in lung adenocarcinoma tissues, and its expression was markedly associated with clinical staging in patients. Moreover, ectopic expression of miR‑888 in vitro was revealed to function as a double‑edged sword in the progression of lung adenocarcinoma A549 cells by targeting multiple targets. Overexpression of miR‑888 promoted the invasion and migration of lung adenocarcinoma A549 cells by targeting E‑cadherin and tissue inhibitor of metalloproteinase 2. In addition, ectopic expression of miR‑888 inhibited the proliferation of lung adenocarcinoma A549 cells by targeting cell division cycle 7 (CDC7). In addition, the immunohistochemical results and The Cancer Genome Atlas (TCGA) database revealed that CDC7 was significantly upregulated in lung adenocarcinoma tissues, suggesting that miR‑888 may function as an oncogene in the progression of lung adenocarcinoma patients, and the miR‑888/CDC7 axis was not the dominant pathway for CDC7 regulation in patients with lung adenocarcinoma. In conclusion, our findings indicated that miR‑888 may act as a potential new therapeutic target for patients with lung adenocarcinoma.