Journal
ONCOTARGET
Volume 8, Issue 19, Pages 30817-30829Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.10339
Keywords
SMAD4; miR-205; NSCLC; proliferation; cell cycle
Categories
Funding
- National Natural Science Foundation of China [81201575, 31270940]
- Science and Technology Committee of Jiangsu Province [BK2012606]
- Jiangsu Province Colleges and Universities Natural Science Research Foundation [12KJB310016, 14KJB0017]
- Foundation of Health Care Rejuvenation by Science and Education [KJXW2011006]
- Clinical Medical Center of Suzhou [Szzx201502]
- Clinical Key Specialty Project of China
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Despite advances in diagnosis and treatment, the survival of non-small cell lung cancer (NSCLC) patients remains poor; therefore, improved understanding of the disease mechanism and novel treatment strategies are needed. Downregulation of SMAD4 and dysregulated expression of miR-205 have been reported. However, the relationship between them remains unclear. We investigated the effect of microRNA (miR)-205 on the expression of SMAD4 in NSCLC. Knockdown and overexpression of SMAD4 promoted or suppressed cellular viability and proliferation, and accelerated or inhibited the cell cycle in NSCLC cells, respectively. The 3'-untranslated region (3'-UTR) of SMAD4 was predicted as a target of miR-205. Luciferase assays validated that miR-205 binds directly to the SMAD4 3'-UTR. Protein and mRNA expression analyses confirmed that miR-205 overexpression in NSCLC cells inhibited the expression of SMAD4 mRNA and protein. In human NSCLC tissues, increased miR-205 expression was observed frequently and was inversely correlated with decreased SMAD4 expression. Ectopic expression of miR-205 in NSCLC cells suppressed cellular viability and proliferation, accelerated the cell cycle, and promoted tumor growth of lung carcinoma xenografts in nude mice. Our study showed that miR-205 decreased SMAD4 expression, thus promoting NSCLC cell growth. Our findings highlighted the therapeutic potential of targeting miR-205 in NSCLC treatment.
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