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MicroRNAs (miRNAs) are a cluster of short non-coding RNAs playing critical roles in human cancers. miR-187 was recently found to be a novel cancer-related microRNA. However, the expression and function of miR-187 in cervical cancer have not been investigated. In this study, we found that miR-187 level was decreased in cervical cancer tissues and cell lines. Patients with low level of miR-187 had significantly decreased rate of overall survival (OS) and progression-free survival (DFS). miR-187 overexpression inhibited proliferation and promoted apoptosis of cervical cancer cells, whereas miR-187 knockdown promoted proliferation and inhibited apoptosis of cervical cancer cells. Forced expression of miR-187 inhibited the subcutaneous growth of cervical cancer cells in nude mice. Furthermore, FGF9 was found to be the downstream target of miR-187 in cervical cancer cells. Importantly, targeting FGF9 was required for miR-187 exerting its tumor suppressive roles in cervical cancer cells.

Cervical cancer (CC) is the fourth most frequent malignancy worldwide. MicroRNAs (miRNAs) can function as potential biomarkers or therapeutic targets in multiple cancers including CC. Our present study aimed to investigate the roles and downstream targets of microRNA-20a (miR-20a) in regulating CC proliferation, apoptosis and autophagy. Here, RT-qPCR assay revealed that miR-20a was highly expressed in CC tissues and cells. Functional analysis showed that the inhibition of miR-20a resulted in reduced proliferation, increased apoptosis and downregulated autophagic activity in CC cells. Bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation (RIP) assay manifested that thrombospondin 2 (THBS2) was a target of miR-20a. Also, THBS2 expression was notably reduced in CC tissues and cells, and inversely associated with miR-20a expression in CC tissues. Restoration experiments disclosed that THBS2 knockdown abrogated miR-20a inhibitor-mediated anti-proliferation, pro-apoptosis, and anti-autophagy effects in CC cells. In summary, these data showed that the depletion of miR-20a suppressed proliferation and autophagy and induced apoptosis by targeting THBS2 in CC cells, further elucidating the roles and molecular basis of miR-20a in the development of CC.

Systemic sclerosis (SSc) is a multisystemic fibrotic disease characterized by excessive collagen deposition and extracellular matrix synthesis. Though transforming growth factor-β (TGF-β) plays a fundamental role in the pathogenesis of SSc, the mechanism by which TGF-β signaling acts in SSc remains largely unclear. Here, we showed that TGF-β type II receptor (TGFBR2) was significantly upregulated in both human SSc dermal tissues and primary fibroblasts. In fibroblasts, siRNA-induced knockdown of TGFBR2 resulted in a reduction of p-SMAD2/3 levels and reduced production of type I collagen. Additionally, functional experiments revealed that downregulation of TGFBR2 yielded an anti-growth effect on fibroblasts through inhibiting cell cycle progression. Further studies showed that miR-3606-3p could directly target the 3'-UTR of TGFBR2 and significantly decrease the levels of both TGFBR2 mRNA and protein. Furthermore, SSc dermal tissues and primary fibroblasts contain significantly reduced amounts of miR-3606-3p, and the overexpression of miR-3606-3p in fibroblasts replicates the phenotype of TGFBR2 downregulation. Collectively, our findings demonstrated that increased TGFBR2 could be responsible for the hyperactive TGF-β signaling observed in SSc. Moreover, we identified a pivotal role for miR-3606-3p in SSc, which acts, at least partly, through the attenuation of TGF-β signaling via TGFBR2 repression, suggesting that the regulation of miR-3606-3p/TGFBR2 could be a promising therapeutic target that could improve the treatment strategy for fibrosis.