MiR-378 Promotes the Migration of Liver Cancer Cells by Down-Regulating Fus Expression

Ma, Ji‐chun; Jiang, Lin; Qian, Jun; Qian, Wei; Yin, Jiayu; Yang, Burton B.; Tang, Qin; Chen, Xingxing; Wen, Xiang‐mei; Guo, Hong; Deng, Zhaoqun

doi:10.1159/000369669

Cited by 45 publications

(33 citation statements)

References 31 publications

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“…Previous study has shown that FUS-binding sites are rich in GU contents and are highly degenerative, and FUS-binding motifs of GGU, GGUG, GUGGU and CGCGC have been previously reported [30], however, the detailed binding sites of FUS on LATS1/2 are still unclear, which would be solved in our future work. It is interesting to note that miR-378 promotes HCC cells migration by down-regulating FUS expression [17], which suggests the inhibitory roles of FUS in HCC migration and this effect is consistent with our results. And since the stemness of cancer cells could confer chemoresistance [31], and FUS expression has been shown to be correlated with cisplatin chemosensitivity in neuroblastoma cell lines [32], future studies could focus on the effects of FUS on chemotherapeutics sensitivity in HCC cells.…”

Section: Discussionsupporting

confidence: 91%

“…And FUS regulates AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor function and FTLD/ALS-associated behaviour via stabilizing GluA1 mRNA [16]. In HCC, miR-378 could promote the migration of HCC cells by down-regulating FUS expression [17], which indicates the inhibitory roles of FUS in HCC progression. However, the expression level, roles and related mechanisms of FUS in HCC progression are still unclear.…”

Section: Introductionmentioning

confidence: 99%

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A FUS-LATS1/2 Axis Inhibits Hepatocellular Carcinoma Progression via Activating Hippo Pathway

Bao

Yuan

et al. 2018

Cell Physiol Biochem

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Background/Aims: The roles and related mechanisms of RNA binding protein FUS (fused in sarcoma/translocated in liposarcoma) are unclear in numerous cancers, including hepatocellular carcinoma (HCC). Methods: Quantitative reverse transcription PCR (qRT-PCR), western blot, cell viability, transwell migration and invasion, tumor spheres formation and in vivo tumor formation assays were used to examine the effects of FUS on HCC progression in HuH7 and MHCC97 cells. Additionally, transcriptome analysis based on RNA-sequencing data, qRT-PCR, western blots, luciferase reporter and RNA binding protein immunoprecipitation (RIP) assays were used to explore the LATS1/2 (large tumor suppressor kinases 1/2)-related mechanisms contributing to FUS functions. Finally, qRT-PCR and western blot analysis were used to detect the levels of FUS and LATS1/2 in HCC and adjacent normal tissues, and the correlation between them in HCC tissues. Results: Overexpression of FUS decreased cell viability, migration, invasion and stemness. Moreover, FUS interacted and stabilized LATS1/2 stability, and thus promoted LATS1/2 expression and activated Hippo pathway. Finally, FUS and LAST1/2 levels were positively correlated and significantly down-regulated in HCC tissues. Conclusion: We demonstrate that FUS/LATS1/2 axis inhibits HCC progression via activating Hippo pathway.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

A FUS-LATS1/2 Axis Inhibits Hepatocellular Carcinoma Progression via Activating Hippo Pathway

Bao

Yuan

et al. 2018

Cell Physiol Biochem

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“…Mature miRNAs derive from a complex process, where a primitive form of miRNA (pri-miR) is transcribed by RNA pol II and cleaved by the ribonuclease DROSHA in the nucleus to originate a precursor miRNA (pre-miR), which is exported to the cytoplasm or the endoplasmic reticulum and undergoes a second cleavage by a RNase III endonuclease, Dicer, to become approximately 22 nucleotides length miRNA duplex [7]. Emerging evidence suggests that miRNAs play critical roles in many cellular processes, including cell growth, invasion, metabolism and differentiation [8][9][10][11]. It was recently revealed that miRNAs have been involved in mediating the osteogenic differentiation of osteoblasts and mesenchymal stem cells (MSCs).…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-Induced MicroRNA-429 Promotes Differentiation of MC3T3-E1 Osteoblastic Cells by Mediating ZFPM2 Expression

Huang

Peng

Cao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Hypoxia has been reported to regulate osteoblastic differentiation of bone cells and cartilage development. However, information concerning the molecular mechanisms remains largely unknown. Methods: The expression of miR-429 was evaluated by quantitative real-time PCR analysis. To test whether miR-429 directly regulate the expression level of ZFPM2 at transcription level, dual-luciferase reporter gene assay was performed. Western blotting was performed to detect osteogenesis related protein expression. The cell proliferation, apoptosis, alkaline phosphatase activity and matrix mineralization were performed to assess the functions of miR-429 in vitro and in vivo the effects of miR-429 on fracture healing. Results: Expression of miR-429 was increased in MC3T3-E1 cells treated with 200 μM CoCl₂ by qRT-PCR, and overexpression of miR-429 promoted cell differentiation, and enhanced alkaline phosphatase activity and matrix mineralization. Luciferase reporter assays suggested that miR-429 directly targets the 3'UTR of ZFPM2. In addition, knockdown of ZFPM2 could phenocopy the effects of miR-429 expression. Furthermore, overexpression of ZFPM2 in miR-429-expressing MC3T3-E1 cells suppressed cell differentiation. Conclusions: Our results provide valuable insight into the potential role of hypoxia in regulation of osteoblastic cell differentiation.

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“…MiR-378 was originally identified as an oncogene promoting VEGF expression in human nasopharyngeal carcinoma, 12 now it has been proved to participate in a variety of biological processes, such as cancer metastasis and differentiation. 13–14 MiR-378 was strongly upregulated during adipogenic differentiation and positively regulated adipogenesis. 15–17 As for osteogenesis, some studies reported that miR-378 promoted osteogenic differentiation, 8 while other study demonstrated that miR-378 suppressed osteogenic differentiation.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-378 suppressed osteogenesis of mesenchymal stem cells and impaired bone formation via inactivating Wnt/β-catenin signaling

Zhang

Shi

et al. 2019

Preprint

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37MicroRNAs (miRNAs) have been reported to serve as silencers to repress gene 38 expression at post-transcriptional level. Multiple miRNAs have been demonstrated to 39 play important roles in osteogenesis. MiR-378, a conserved miRNA, was reported to 40 mediate bone metabolism and influence bone development, but the detailed function 41 and underlying mechanism remain obscure. In this study, the miR-378 transgenic (TG) 42 mouse was developed to study the role of miR-378 in osteogenic differentiation as 43 well as bone formation. The abnormal bone tissues and impaired bone quality were 44 displayed in the miR-378 TG mice, and a delayed healing effect was observed during 45 bone fracture of the miR-378 TG mice. The osteogenic differentiation of MSCs 46 derived from this TG mouse was also inhibited. We also found that miR-378 mimics 47 suppressed while anti-miR-378 promoted osteogenesis of human MSCs. Two Wnt 48 family members Wnt6 and Wnt10a were identified as bona fide targets of miR-378, 49 and their expression were decreased by this miRNA, which eventually induced the 50 inactivation of Wnt/β-catenin signaling. Finally, the sh-miR-378 modified MSCs were 51 locally injected into the fracture sites in an established mouse fracture model. The 52 results indicated that miR-378 inhibitor therapy could promote bone formation and 53 stimulate healing process in vivo. In conclude, miR-378 suppressed osteogenesis and 54 bone formation via inactivating Wnt/β-catenin signaling, suggesting miR-378 may be 55 a potential therapeutic target for bone diseases.56 Key words: miR-378; mesenchymal stem cells; osteogenesis; Wnt/β-catenin 57 signaling; bone formation 58 59 Bone regeneration is very important for the recovery of some diseases including 60 osteoporosis and bone fracture trauma. It is a multiple step and multiple gene involved 61 complex process, including osteoblast-mediated bone formation and 62 osteoclast-mediated bone resorption. During this process, mesenchymal stem cells 63 (MSCs) gradually differentiate into osteoblasts, which produce a variety of 64 extracellular matrix and thus induce the initiation of bone formation. Hence, 65 improving the osteoblast differentiation of MSCs is crucial for the development of 66 therapeutic strategy for bone diseases. 67 Over the past few years, microRNAs (miRNAs) have emerged as gene silencers to 68 suppress gene expression at post-transcriptional level. Multiple miRNAs have been 69 demonstrated to play important roles in biological activities including osteogenic 70 differentiation and skeletal development. For example, miR-26a, miR-29b, miR-125b, 71 miR-133, miR-135 and miR-196a, have been reported to be involved in 72 osteogenesis. 1-5 Our previous reports also demonstrated that miR-20a and 20b 73 promoted whereas miR-637 suppressed osteoblast differentiation. 6-7 Therefore, 74 miRNAs have been considered as potential candidates to mediate osteogenic 75 differentiation and may be acted as therapeutic targets for bone regeneration.76 MiR-378, which is derived from a ...

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MiR-378 Promotes the Migration of Liver Cancer Cells by Down-Regulating Fus Expression

Cited by 45 publications

References 31 publications

A FUS-LATS1/2 Axis Inhibits Hepatocellular Carcinoma Progression via Activating Hippo Pathway

A FUS-LATS1/2 Axis Inhibits Hepatocellular Carcinoma Progression via Activating Hippo Pathway

Hypoxia-Induced MicroRNA-429 Promotes Differentiation of MC3T3-E1 Osteoblastic Cells by Mediating ZFPM2 Expression

MicroRNA-378 suppressed osteogenesis of mesenchymal stem cells and impaired bone formation via inactivating Wnt/β-catenin signaling

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