miR‐4319 inhibited the development of thyroid cancer by modulating FUS‐stabilized SMURF1

Bian, Shuquan

doi:10.1002/jcb.29026

Cited by 33 publications

(22 citation statements)

References 22 publications

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“…Combined with results from starBase and our experiments, FUS was identified as the RBP for LDHB. RBP FUS has been discovered to act as a tumor enhancer in several cancers such as thyroid cancer, non-small cell lung cancer and glioma [26][27][28]. Apart from the verified affinity between FUS and LDHB, it was also revealed that FUS could elevate the stability of LDHB mRNA.…”

Section: Discussionmentioning

confidence: 99%

MiR-141-3p overexpression suppresses the malignancy of osteosarcoma by targeting FUS to degrade LDHB

Wang

2020

Bioscience Reports

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Osteosarcoma (OS) is a common malignant bone cancer. Lactate dehydrogenase B (LDHB) has been revealed to act as a tumor promoter in several cancers. It is also revealed to be correlated with poor prognosis in OS, but its molecular mechanism in OS remains veiled. Our work illustrated that LDHB was overexpressed in OS tissues and cells, and it could enhance cell proliferation, migration, and invasion in OS. Subsequently, it was confirmed that fused in sarcoma (FUS) could bind with LDHB to positively regulate the stability of LDHB messenger RNA (mRNA). Besides, FUS expression was revealed to be elevated in OS tissues and positively correlate with LDHB expression. Furthermore, miR-141-3p, down-regulated in OS cells, was identified as the upstream regulator of FUS in OS cells. Besides, miR-141-3p overexpression decreased mRNA and protein levels of FUS and LDHB. More importantly, overexpression of miR-141-3p could impair FUS overexpression-mediated promotion on LDHB mRNA stability and expression. Finally, rescue assays indicated that miR-141-3p regulated OS cells cellular process via regulating LDHB. In sum, miR-141-3p targets FUS to degrade LDHB, thereby attenuating the malignancy of OS cells.

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Section: Discussionmentioning

confidence: 99%

MiR-141-3p overexpression suppresses the malignancy of osteosarcoma by targeting FUS to degrade LDHB

Wang

2020

Bioscience Reports

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“…MicroRNAs (miRNAs) are a group of small singlestranded RNAs consisting of 22 nucleotides with a typical hairpin secondary structure [7]. They modulate gene silencing via directly targeting at an mRNA for degeneration or repressing translation [8]. A change in miRNA expression is related to different kinds of malignancies, such as EOC [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-145-5p regulates the proliferation of epithelial ovarian cancer cells via targeting SMAD4

Zhou¹,

Zhang²,

Li³

et al. 2020

J Ovarian Res

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Background: Epithelial ovarian cancer (EOC) is one of the most prevalent malignancies affecting females worldwide; however, its etiology mechanism remains unclear. In various malignancies, miR-145-5p is a widely accepted and versatile miRNA. Therefore, our research focused on exploring the activity and etiology of miR-145-5p in the modulation of metastasis, migration, and proliferation of EOC cells. The direct reactions between the 3′UTRs of SMAD4 mRNA and miR-145-5p were verified using dual luciferase reporter test. SKOV-3 cells were subsequently transfected using miR-145-5p mimics. Cell migration, death, and proliferation were evaluated using MTT, flow cytometry, and Transwell test. In addition, SMAD4 transcription and translation were evaluated using qRT-PCR and Western blot. Results: We found that miR-145-5p expression was repressed prevalently in EOC tissues, apart from SMAD4 upregulation. Excessive miR-145-5p expression remarkably reinforced EOC cell death and repressed EOC cell proliferation. Furthermore, upregulated miR-145-5p expression noticeably repressed migration via MMP-2 and MMP-9 downregulation. Moreover, SMAD4 was downregulated via miR-145-5p transfection. The dual luciferase test revealed that miR-145-5p directly targeted SMAD4. Conclusions: Our research suggests that miR-145-5p serves as a malignancy repressor and exerts an essential impact on inhibiting malignancy generation and reinforcing EOC death via targeting SMAD4. MiR-145-5p application could serve as a promising strategy to treat EOC.

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“…Moreover, miR-4319 is transcriptionally modulated by PLZF and acts as a tumour suppressor in CRC (colorectal cancer) via targeting ABTB1 21. MiR-4319 suppresses the development of thyroid cancer by regulating FUS (fused in sarcoma)-stabilized SMURF1 (SMAD-specific E3 ubiquitin protein ligase 1) 25. Nevertheless, the biological effects and the latent regulatory mechanism of miR-4319 in HCC remain obscure and need to be further elucidated.…”

Section: Introductionmentioning

confidence: 99%

MiR-4319 induced an inhibition of epithelial-mesenchymal transition and prevented cancer stemness of HCC through targeting FOXQ1

et al. 2019

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The heterogeneity existing in tumours is responsible for the poor response to treatment. Therefore, elucidating the molecular mechanisms of intratumoural heterogeneity in hepatocellular carcinoma (HCC) is vital for the discovery of new therapeutic methods for improving the prognosis of patients. Of note, cancer stem cells (CSCs) existing in HCC may explain the pathological properties of heterogeneity and recurrence. An increasing number of studies have confirmed that abnormally expressed microRNAs (miRNAs) take part in the carcinogenesis as well as the aggravation of HCC. However, little information is currently available about the specific miR-4319 in HCC. Herein, we demonstrated that the level of miR-4319 was remarkably decreased in HCC specimens and cells compared to that in normal counterparts and that the depression of miR-4319 in tumour specimens correlates with tumour size, histological grade and venous invasion. Through a series of functional experiments, we illustrated that miR-4319 repressed cell proliferation, accelerated apoptosis, inhibited epithelial-mesenchymal transition (EMT) and prevented cancer stemness in HCC cells by targeting FOXQ1 (Forkhead box Q1). An in vivo tumourigenesis assay uncovered that depletion of miR-4319 in Hep3B cells increased tumour growth and elevated the expression of EMT and CSC markers in comparison to those of the control group. Restoration of FOXQ1 expression also partially reversed the miR-4319-induced biological effects on HCC cells. Thus, miR-4319, as a posttranscriptional regulator, plays a profound role in suppressing the malignant progression of HCC, and our study highlights the miR-4319/FOXQ1 cascade as a potential therapeutic target for conquering HCC.

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miR‐4319 inhibited the development of thyroid cancer by modulating FUS‐stabilized SMURF1

Cited by 33 publications

References 22 publications

MiR-141-3p overexpression suppresses the malignancy of osteosarcoma by targeting FUS to degrade LDHB

MiR-141-3p overexpression suppresses the malignancy of osteosarcoma by targeting FUS to degrade LDHB

MicroRNA-145-5p regulates the proliferation of epithelial ovarian cancer cells via targeting SMAD4

MiR-4319 induced an inhibition of epithelial-mesenchymal transition and prevented cancer stemness of HCC through targeting FOXQ1

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