MicroRNA-30a-5p (miR-30a) regulates cell motility and EMT by directly targeting oncogenic TM4SF1 in colorectal cancer

Park, Y. R.; Kim, S. W.; Lee, M. R.; Seo, Seung Young; Lee, J. H.; Kim, I. H.; Lee, S. O.; Kim, Sang Wook

doi:10.1007/s00432-017-2440-4

Cited by 51 publications

(40 citation statements)

References 38 publications

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“…Increasing evidence demonstrates that restoration of miR-30a contributes to the suppression of EMT process in various cancers and fibrotic diseases [24, 34, 35], indicating an inhibitory role of miR-30a in EMT. Generally, TGF-β1, Vimentin, E-cadherin and GFAP are considered to be important EMT markers.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-30a Suppresses the Activation of Hepatic Stellate Cells by Inhibiting Epithelial-to-Mesenchymal Transition

Zheng¹,

Wang²,

Yu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The activation of hepatic stellate cells (HSCs) is considered as a pivotal event in liver fibrosis and epithelial-mesenchymal transition (EMT) process has been reported to be involved in HSC activation. It is known that microRNAs (miRNAs) play a pro-fibrotic or anti-fibrotic role in HSC activation. Recently, emerging studies show that miR-30a is down-regulated in human cancers and over-expression of miR-30a inhibits tumor growth and invasion via suppressing EMT process. However, whether miR-30a could regulate EMT process in HSC activation is still unclear. Methods: miR-30a expression was quantified using real-time PCR in carbon tetrachloride (CCl₄)-induced rat liver fibrosis, activated HSCs and patients with cirrhosis. Roles of miR-30a in liver fibrosis in vivo and in vitro were also analyzed. Luciferase activity assays were performed to examine the binding of miR-30a to the 3′-untranslated region of snail family transcriptional repressor 1 (Snai1). Results: miR-30a was down-regulated in human cirrhotic tissues. In CCl₄ rats, reduced miR-30a was found in fibrotic liver tissues as well as isolated HSCs. There was a significant reduction in miR-30a in primary HSCs during culture days. miR-30a over-expression resulted in the suppression of CCl₄-induced liver fibrosis. Restoration of miR-30a led to the inhibition of HSC activation including cell proliferation, α-SMA and collagen expression. Notably, miR-30a inhibited EMT process, with a reduction in TGF-β1 and Vimentin as well as an increase in GFAP and E-cadherin. miR-30a induced a significant reduction in Snai1 protein expression when compared with the control. Interestingly, Snail protein expression was increased during liver fibrosis, indicating that there may be a negative correlation between miR-30a level and Snai1 protein expression. Further studies demonstrated that Snai1 was a target of miR-30a. Conclusion: Our results suggest that miR-30a inhibits EMT process, at least in part, via reduction of Snai1, leading to the suppression of HSC activation in liver fibrosis.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-30a Suppresses the Activation of Hepatic Stellate Cells by Inhibiting Epithelial-to-Mesenchymal Transition

Zheng¹,

Wang²,

Yu³

et al. 2018

Cell Physiol Biochem

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“…Other experiments showed that miR-483 could inhibit cell proliferation in Polycystic Ovarian Syndrome via Targeting Insulin-Like Growth Factor 1 (IGF1) [17]. Although there are many studies on microRNA and colon cancer, such as mir-30a-5p (miR-30a) regulates cell motility and EMT by targeting TM4SF1 in colorectal cancer [18]. MiR-944 inhibits cell migration and invasion by targeting MACC1 in colorectal cancer [19].…”

Section: Discussionmentioning

confidence: 99%

Mir‐483 inhibits colon cancer cell proliferation and migration by targeting TRAF1

Niu

Jiang

et al. 2018

The Kaohsiung J of Med Scie

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MicroRNAs are important regulators during human growth and development. Emerging evidence indicates that microRNAs play important roles in colorectal cancer. The aim of this study is to reveal the biological function and direct target gene of miR-483 in colorectal cancer. The biological function of miR-483 on the proliferation and migration of colon cancer cells was then examined by Edu assay and transwell assay, respectively. Our findings revealed that miR-483 mimic could significantly inhibit cell proliferation and migration. The target gene of miR-483 was predicted by target scan software and identified by a dual fluorescence reporter system which showed that TRAF1 was a direct target gene of miR-483 in SW480 cell line. These data suggest that miR-483 is a colorectal cancer suppressor which could inhibit cell proliferation and migration, possibly via targeting TRAF1. The miR-483 could be a potential treatment target for colorectal cancer.

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“…[32][33][34] Recent studies have examined the correlation of TM4SF1 with microRNAs in tumor angiogenesis of various cancers. 35,36 TM4SF1 is reportedly one of the candidate markers of thyroid cancer stem cells; however, its clinical application needs to be studied further. 37 There are no existing scientific studies of TM4SF1 expression in thyroid cancer tissue.…”

Section: F I G U R E 3 Validation Of Microarray-based Gene Expressionmentioning

confidence: 99%

Extensive lymphatic spread of papillary thyroid microcarcinoma is associated with an increase in expression of genes involved in epithelial‐mesenchymal transition and cancer stem cell‐like properties

et al. 2019

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BackgroundActive surveillance is an alternative management for patents with low‐risk papillary thyroid microcarcinoma (PTMC); however, there is an absence of specific molecular markers that predict its progression. We compared gene expression patterns between PTMC with lateral neck‐node metastasis (N1b) and PTMC‐lacking nodal metastasis (N0).MethodsWe performed oligonucleotide microarray analysis in three PTMCs without cervical lymph‐node metastases (N0), and five PTMCs with lateral neck‐node metastasis (N1b) at initial diagnosis, using an Illumina HumanHT‐12 v4.0 Expression BeadChip. Quantitative real‐time PCR (qPCR) and western blot analysis confirmed microarray data. We performed immunohistochemistry (IHC) to confirm protein overexpression in samples from 20 N0 and 24 N1b PTMC patients who underwent thyroidectomy.ResultsMicroarray analyses identified 52 probes corresponding to 45 genes. Expression of these genes differed significantly between the two PTMC groups. Forty genes were significantly upregulated and five genes were downregulated in N1b PTMC compared to N0. Four genes related to epithelial‐to‐mesenchymal transition (EMT) and stem cell markers, including ALDH1A3, TM4SF1, PROM1, and CAV1 were significantly upregulated in N1b PTMCs. Real‐time qPCR confirmed this expression and western blot analysis confirmed higher expression of ALDH1A3, TM4SF1, PROM1, and CAV1 in N1b than in N0 PTMCs. IHC indicated overexpression of ALDH1A3 and CAV1 in N1b compared to N0 PTMCs.ConclusionsGenes related to EMT and thyroid cancer stem cell‐like properties are upregulated in early extensive lymphatic spread of PTMC.

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MicroRNA-30a-5p (miR-30a) regulates cell motility and EMT by directly targeting oncogenic TM4SF1 in colorectal cancer

Abstract: These results suggest that miR-30a is an important regulator of TM4SF1, VEGF, and E-cadherin for CRC lymph node metastasis, a potential new therapeutic target in CRC.

Cited by 51 publications

References 38 publications

MicroRNA-30a Suppresses the Activation of Hepatic Stellate Cells by Inhibiting Epithelial-to-Mesenchymal Transition

MicroRNA-30a Suppresses the Activation of Hepatic Stellate Cells by Inhibiting Epithelial-to-Mesenchymal Transition

Mir‐483 inhibits colon cancer cell proliferation and migration by targeting TRAF1

Extensive lymphatic spread of papillary thyroid microcarcinoma is associated with an increase in expression of genes involved in epithelial‐mesenchymal transition and cancer stem cell‐like properties

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