Journal
CANCER SCIENCE
Volume 109, Issue 2, Pages 289-296Publisher
WILEY
DOI: 10.1111/cas.13452
Keywords
Cell proliferation; miR-335; non-small cell lung cancer; prognosis; Tra2
Categories
Funding
- Six talent peaks project in Jiangsu Province, China [WSN-059]
- Science Foundation of Nantong City, Jiangsu, China [MS12015007]
- Scientific research topic of Jiangsu provincial health and Family Planning Commission, China [H201626]
- Key talents of Medical Science in Jiangsu Province, China [QNRC2016682]
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Accumulating evidence has suggested that the dysregulation of miRNA is an important factor in the pathogenesis of lung cancer. Here, we demonstrate that miR-335 expression is reduced in non-small cell lung cancer (NSCLC) tumors relative to non-cancerous adjacent tissues, while the expression of Tra2 is increased. In addition, clinical data revealed that the increased Tra2 and decreased miR-335 expression observed in NSCLC cells was associated with poor patient survival rates. In vitro experimentation showed that the overexpression of miR-335 inhibited the growth, invasion and migration capabilities of A459 lung cancer cells, by targeting Tra2. In contrast, inhibition of miR-335 or overexpression of the Tra2 target gene stimulated the growth, invasion and migratory capabilities of A459 lung cancer cells in vitro. Furthermore, overexpression of miR-335 or inhibition of Tra2 decreased the phosphorylation of Rb-S780 and Rb-AKT. Overall, these findings suggest that the downregulation of miR-335 in A459 lung cancer cells promoted cell proliferation through upregulation of Tra2, mediated via activation of the AKT/mTOR signaling pathway, and suggest that miR-335 may have potential as a novel therapeutic target for NSCLC.
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