miR-187-3p inhibits the metastasis and epithelial–mesenchymal transition of hepatocellular carcinoma by targeting S100A4

Dou, Changwei; Liu, Zhikui; Xu, Meng; Jia, Yuli; Wang, Yufeng; Li, Qing; Yang, Wei; Zheng, Xin; Tu, Kangsheng; Liu, Qingguang

doi:10.1016/j.canlet.2016.08.011

Cited by 90 publications

(74 citation statements)

References 50 publications

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“…Beside the reports about its transcriptional regulation the post-transcriptional regulation of S100A4 is not well understood. miR-187-3p is reported to post-transcriptionally regulate S100A4 and S100A4-mediated metastasis in hepatocellular carcinoma (HCC) [22]. Here we demonstrate that loss of post-transcriptional regulation of S100A4 due to epigenetic silencing of miR-505-5p and miR-520c-3p expression could be one of the main causes for the induction of S100A4 expression in CRC and other cancer entities.…”

Section: Discussionmentioning

confidence: 60%

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Epigenetic silencing of miR-520c leads to induced S100A4 expression and its mediated colorectal cancer progression

et al. 2017

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The S100 calcium-binding protein A4 (S100A4) induces epithelial mesenchymal transition, migration, invasion, angiogenesis and metastasis. Its induced expression in several cancer types correlates with poor prognosis. Apart from the functional and transcriptional regulatory aspects of S100A4, its post-transcriptional regulation is not yet clearly elucidated. In this study, we show that microRNAs (miR) miR-505-5p and miR-520c-3p target the 3′-UTR of S100A4 and inhibits its expression and its mediated migration and invasion. 5-Aza treatment significantly increased miR-520c-3p expression and reduced the S100A4 protein amounts. The upstream promoter region of miR-520c is hypermethylated irrespective of the metastasis status of colorectal cancer (CRC) patient tissues and in all analyzed CRC cell lines. Moreover, in a cohort of CRC patient specimen (n = 59), miR-520c-3p was significantly downregulated. miR-520c-3p stably expressing HCT116 cells showed a reduced metastasis formation in livers after implanting in mice spleen. Taken together, our findings demonstrate that S100A4 is post-transcriptionally regulated by tumor suppressor miRs, miR-505c-5p and miR-520c-3p, and particularly miR-520c-3p expression is epigenetically silenced in CRC.

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Section: Discussionmentioning

confidence: 60%

“…Moreover, its induced expression is positively correlated with tumor progression, metastasis and poor survival of patients [6, 21]. However, to our knowledge only miR-187-3p is reported to post-transcriptionally regulate S100A4 and S100A4 mediated metastasis [22]. This was so far only shown in hepatocellular carcinoma (HCC).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic silencing of miR-520c leads to induced S100A4 expression and its mediated colorectal cancer progression

et al. 2017

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“…At least two microRNAs that can inhibit S100A4 have been reported: miR‐21 in endothelial cells and miR‐187‐3p in hepatocellular carcinoma . Although these studies used other cellular models, these signals may share phenomena with our miR‐124 /S100A4 in VSMCs to reduce cell survival, suggesting that these microRNAs might also play a key role in neointimal proliferation.…”

Section: Discussionmentioning

confidence: 99%

The microRNA miR‐124 inhibits vascular smooth muscle cell proliferation by targeting S100 calcium‐binding protein A4 (S100A4)

et al. 2017

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S100 calcium-binding protein A4 (S100A4) induces proliferation and migration of vascular smooth muscle cells (VSMCs). We aimed to find the microRNA regulating S100A4 expression. S100A4 transcripts are abruptly increased in the acute phase of carotid arterial injury 1 day later (at day 1) but gradually decreases at days 7 and 14. Bioinformatics analysis reveals that miR-124 targets S100A4. VSMC survival is attenuated by miR-124 mimic but increased by miR-124 inhibitor. miR-124 decreases immediately after carotid arterial injury but dramatically increases at days 7 and 14. miR-124 inhibitor-induced cell proliferation is blocked by S100A4 siRNA, whereas miR-124-induced cell death is recovered by S100A4. Our findings suggest that miR-124 is a novel regulator of VSMC proliferation and may play a role in the development of neointimal proliferation.

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“…Previous studies have causally linked individual microRNA expression changes to adverse biologic processes in HCC, including rapid proliferation, epithelial‐to‐mesenchymal transition (EMT), local tissue invasion, and vascular invasion . A summary of recently published studies with purported miRNA mechanisms is provided in Table . For the majority of cases, miRNA loss correlates to induction of a target oncogene, and miRNA gain correlates to repression of a target tumor suppressor.…”

Section: Microrna Hcc Subtypingmentioning

confidence: 99%

Molecular signatures in hepatocellular carcinoma: A step toward rationally designed cancer therapy

Erstad

Fuchs

Tanabe

2018

Cancer

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Molecular characterization of hepatocellular carcinoma (HCC) has greatly improved our understanding of disease pathogenesis. Mutational analysis, RNA and microRNA expression profiling, and epigenetic characterization have revealed common aberrations in oncogenes and tumor suppressors that correlate with disease biology and serve as a guide for the rational design of targeted therapies. These approaches have also led to the discovery of novel targets, including mutations in isocitrate dehydrogenase and chromatin remodeling enzymes. With the advent of immunotherapy, RNA expression profiling of the tumor microenvironment has identified a subset of HCC with high lymphocyte infiltration that may benefit from checkpoint inhibitor therapy. Molecular signatures thus capture the biology of a tumor, providing a supplement to current staging schema, which are based on tumor size and number, for more accurate prognostication of recurrence risk and survival. Molecular signatures may also be used to guide interventional therapy by defining those most suitable for transplantation or locoregional therapy rather than surgical resection. Finally, a multiomics approach involves the aggregation and analysis of multiple signatures for a more comprehensive characterization of pathogenic mechanisms. This broader approach attempts to address issues with signaling pathway cross-talk and redundancy, which have greatly limited the potential value of targeted therapies to date. Cancer 2018. © 2018 American Cancer Society.

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miR-187-3p inhibits the metastasis and epithelial–mesenchymal transition of hepatocellular carcinoma by targeting S100A4

Cited by 90 publications

References 50 publications

Epigenetic silencing of miR-520c leads to induced S100A4 expression and its mediated colorectal cancer progression

Epigenetic silencing of miR-520c leads to induced S100A4 expression and its mediated colorectal cancer progression

The microRNA miR‐124 inhibits vascular smooth muscle cell proliferation by targeting S100 calcium‐binding protein A4 (S100A4)

Molecular signatures in hepatocellular carcinoma: A step toward rationally designed cancer therapy

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