MicroRNA-130a is upregulated in colorectal cancer and promotes cell growth and motility by directly targeting forkhead box F2
- Wenzhong Chen
- Kehui Tong
- Jiren Yu
Published online on: August 16, 2017
Copyright: © Chen et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Colorectal cancer (CRC) is one of the most prevalent cancers among males and females worldwide. Despite progress in diagnostic and therapeutic strategies for CRC patients, the prognosis for patients with advanced CRC remains poor. MicroRNAs (miRNAs/miRs) are a class of highly conserved short, endogenously expressed and single‑stranded non‑coding RNAs. In recent years, increasing studies have demonstrated that dysregulation of miRNAs is closely associated with CRC carcinogenesis and progression. The aim of the present study was to explore the expression, roles and underlying molecular mechanism of miR‑130a in CRC. The results indicated that miR‑130a was significantly upregulated in CRC, and that miR‑130a expression levels were correlated with TNM stage and lymph node metastasis of CRC. Inhibition of miR‑130a markedly suppressed colorectal cancer cell proliferation, migration and invasion. Furthermore, forkhead box F2 (FOXF2) was identified as a direct downstream target gene of miR‑130a in colorectal cancer. Downregulation of FOXF2 could partially reverse the functions induced by miR‑130a under‑expression in CRC cells. These findings suggested that miR‑130a can regulate FOXF2 and function as an oncogene in CRC. Therefore, miR‑130a may serve as a useful therapeutic agent for miRNA‑based CRC targeted therapy.