microRNA‐497 inhibits invasion and metastasis of colorectal cancer cells by targeting vascular endothelial growth factor‐A

Qiu, Yanyan; Yu, Hui; Shi, Xiaojing; Xu, Ke; Tang, Qingfeng; Liang, Bo; Hu, Song-Jiao; Bao, Yi-Jie; Xu, Jianhua; Cai, Jie; Peng, Wen; Cao, Qing; Yin, Peihao

doi:10.1111/cpr.12237

Cited by 39 publications

(33 citation statements)

References 40 publications

(38 reference statements)

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“…Noteably, although NF90 protein functions as a negative regulator in miRNA biogenesis, so far there is no reports about others miR which could regulate NF90. But there are several miRNAs, 34, 35, 36 which could regulate VEGF and they express/modulate in CRC.…”

Section: Discussionmentioning

confidence: 99%

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

et al. 2016

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Altered expression of microRNA-590-5p (miR-590-5p) is involved in tumorigenesis, however, its role in colorectal cancer (CRC) remains to be determined. In this study, we focused on examining the effects of different expression levels of miR-590-5p in cancer cells and normal cells. Results showed that there are lower expression levels of miR-590-5p in human CRC cells and tissues than in normal control cells and tissues. Similarly, in our xenograft mouse model, knockdown of miR-590-5p promoted the progression of CRC. However, an overexpression of miR-590-5p in the mice inhibited angiogenesis, tumor growth, and lung metastasis. Nuclear factor 90 (NF90), a positive regulator of vascular endothelial growth factor (VEGF) mRNA stability and protein synthesis, was shown to be a direct target of miR-590-5p. The overexpression of NF90 restored VEGFA expression and rescued the loss of tumor angiogenesis caused by miR-590-5p. Conversely, the NF90-shRNA attenuated the increased tumor progression caused by the miR-590-5p inhibitor. Clinically, the levels of miR-590-5p were inversely correlated with those of NF90 and VEGFA in CRC tissues. Furthermore, knockdown of NF90 lead to a reduction of pri-miR-590 and an increase of mature miR-590-5p, suggesting a negative feedback loop between miR-590-5p and NF90. Collectively, these data establish miR-590-5p as an anti-onco-miR that inhibits CRC angiogenesis and metastasis through a new mechanism involving NF90/VEGFA signaling axis, highlighting the potential of miR-590-5p as a target for human CRC therapy.

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Section: Discussionmentioning

confidence: 99%

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

et al. 2016

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“…MicroRNAs (miRNAs) are an abundant class of small, endogenous, single-stranded and noncoding RNAs that modulate gene expression posttranscriptionally through binding to the 3'UTR (3'-untranslated region) of the target gene [14][15][16][17]. MiRNAs participate in many biological processes including cell apotosis, development, proliferation, differentiation, fat metabolism, migration and stress resistance [18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

Wang¹,

Peng²,

Gong³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidences suggest that dysregulated expression of miRNAs contributes to the progression of various tumors. However, the underlying function of miR-423-5p in osteosarcoma remains unexplored. Methods: The expression of miR-423-5p and STMN1 were determined in osteosarcoma samples and cell lines via quantitative real-time PCR. Colony formation and Cell Counting Kit-8 (CCK-8) assays were performed to measure cell proliferation ability and transwell analysis was used to detect cell invasion, and dual luciferase reporter assay was perform to analysis the interaction between the miR-423-5p and STMN1. Results: The expression levels of miR-423-5p and STMN1 in the osteosarcoma tissues and cell lines were measured by qRT-PCR. Cell viability was determined using the clone formation and CCK-8 assays. A dual-luciferase reporter and Western blot were performed to stdudy the target gene of miR-423-5p. Here, we showed that miR-423-5p expression was downregulated in osteosarcoma tissues and cell lines. However, the expression of stathmin1 (STMN1) was downregulated in osteosarcoma tissues and cell lines. Moreover, STMN1 expression level was negatively correlated with the miR-423-5p expression in the osteosarcoma tissues. We identified STMN1 was a direct target gene of miR-423-5p in osteosarcoma cell. Overexpression of miR-423-5p inhibited osteosarcoma cell proliferation, colony formation and invasion. Furthermore, we demonstrated that STMN1 was involved in miR-423-5p-mediated cell behavior such as cell proliferation, colony formation and invasion in the osteosarcoma cell. Conclusion: Our present study indicated that miR-423-5p acted as a tumor suppressor gene in osteosarcoma partly through inhibiting STMN1 expression.

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“…microRNAs (miRNAs) are a class of noncoding, short (19‐23 nucleotides), and endogenous RNAs that involve in gene expression at the post‐transcriptional level . miRNAs play crucial roles in many biological processes, such as cell development, growth, migration, apoptosis, differentiation, and invasion .…”

Section: Introductionmentioning

confidence: 99%

miR‐384 suppressed renal cell carcinoma cell proliferation and migration through targeting RAB23

Liu

Feng

et al. 2018

J of Cellular Biochemistry

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microRNAs (miRNAs) are noncoding, short, and endogenous RNAs that play crucial roles in tumor progression at the post‐transcriptional level. Here, we studied the role of miR‐384 in the pathogenesis of renal cell carcinoma (RCC). We demonstrated that miR‐384 expression was downregulated in the RCC specimens compared with nontumor specimens. Moreover, we showed that RAB23 expression was upregulated in the RCC tissues compared with nontumor tissues. Furthermore, we demonstrated that low expression of miR‐384 was correlated with high levels of RAB23 in RCC tissues. We also demonstrated that the RAB23 was a direct target gene of miR‐384 in RCC cells. In addition, overexpression of miR‐384 suppressed RCC cell proliferation, cell cycle, and cell migration. Furthermore, ectopic expression of RAB23 promoted RCC cell proliferation, cell cycle, and cell migration. These data suggested that miR‐384 played a tumor suppressor microRNA in the development of RCC partly through inhibiting RAB23 expression.

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microRNA‐497 inhibits invasion and metastasis of colorectal cancer cells by targeting vascular endothelial growth factor‐A

Abstract: Thus our results provide evidence that miR-497 might function as a metastasis suppressor in CRC. Targeting miR-497 may provide a strategy for blocking its metastasis.

Cited by 39 publications

References 40 publications

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

miR-423-5p Inhibits Osteosarcoma Proliferation and Invasion Through Directly Targeting STMN1

miR‐384 suppressed renal cell carcinoma cell proliferation and migration through targeting RAB23

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