Research paperThe long non-coding RNA MIAT regulates zinc finger E-box binding homeobox 1 expression by sponging miR-150 and promoteing cell invasion in non-small-cell lung cancer

- The expression of MIAT in NSCLC tissues was upregulated.
- Knockdown of MIAT inhibited the invasive ability of NSCLC cells.
- Knockdown of MIAT downregulated the expression of ZEB1.
- MIAT regulated ZEB1 expression through sponging microRNA (miR)-150.

The myocardial infarction associated transcript (MIAT), a long non-coding RNA (lncRNA), was originally identified as a candidate gene for myocardial infarction, and was recently shown to participate in the progression of cancer and the process of metastasis. However, the biological role of MIAT and the underlying mechanisms that mediate its role in non-small-cell lung cancer (NSCLC) remain unclear. Here, we have shown that the expression of MIAT in NSCLC tissues was upregulated. Knockdown of MIAT substantially inhibited the invasive ability of NSCLC cells. Moreover, the knockdown of MIAT significantly downregulated the expression of the zinc finger E-box binding homeobox 1 (ZEB1), that was upregulated in NSCLC and that promoted cell invasion. Rather than by direct interactions, we found that MIAT indirectly regulated ZEB1 expression through sponging and suppressing microRNA (miR)-150, which represses ZEB1 and interacts with MIAT in a sequence-specific manner. Thus, MIAT may inhibit ZEB1 expression and promote cell invasion of NSCLC cells via the miR-150/ZEB1 pathway. Taken together, our findings suggested that MIAT plays an oncogenic role in NSCLC through the ZEB1 signaling pathway by sponging miR-150, and MIAT may therefore serve as a valuable prognostic biomarker and therapeutic target for NSCLC.