<scp>LINC</scp>00473 antagonizes the tumour suppressor miR‐195 to mediate the pathogenesis of Wilms tumour via <scp>IKK</scp>α

Zhu, Shi-En; Fu, Wen; Zhang, Liyu; Fu, Kai; Hu, Jinhua; Jia, Wei Hua; Liu, Guo-chang

doi:10.1111/cpr.12416

Cited by 74 publications

(78 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…7 Moreover, LINC00473, as an oncogene, is upregulated to participate in the progression of WT via miR-195/IKKα. 8 Wang et al have demonstrated that miR-194-5p inhibits cell migration and invasion via directly targeting E2F3 in bladder cancer. 9 MiR-194-5p was reported to inhibit EMT by reducing E-cadherin and inhibited cell migration, invasion, and metastasis in gastric cancer, metrocarcinoma, and liver cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Retracted: MiR‐194‐5p inhibited metastasis and EMT of nephroblastoma cells through targeting Crk

Liu

Ren

Qü

et al. 2019

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

Wilms tumor (WT) is the most common solid childhood tumors all over the world. MicroRNAs (miRs) contribute to tumorigenesis of various cancers through targeting gene. The present study investigated the vital role of miR‐194‐5p and its underlying mechanism in the progression of WT. Immunohistochemistry and quantitative real‐time polymerase chain reaction (qRT‐PCR) assay indicated downregulation of miR194‐5p and upregulation of Crk, in WT tissues compared to adjacent normal tissues. Transfection with miR‐194‐5p mimics into nephroblastoma cells showed a significant decline in cell migration and invasion, which was detected by Transwell assay. Luciferase assay confirmed that Crk was a direct target gene of miR‐194‐5p. More important, the mesenchymal to epithelial transition (EMT) biomarkers containing E‐cadherin, N‐cadherin and Zeb1 were examined by Western blot, and revealed that miR‐194‐5p mimics decreased the levels of N‐cadherin and Zeb1 but increased E‐cadherin, which suggested that miR‐194‐5p inhibited EMT. Crk knockdown could reverse the increased nephroblastoma cell invasion, migration and EMT caused by miR‐194‐5p inhibitor. Interestingly, qRT‐PCR and Western blot analysis showed that overexpression of miR‐194‐5p deactivated HGF/c‐Met/Scr signaling pathway via targeting Crk. In conclusion, miR‐194‐5p inhibited nephroblastoma cell metastasis and EMT in the progression of WT by targeting Crk. Thus, miR‐194‐5p might be a potential target in WT particularly for the prevention of metastasis and EMT.

show abstract

Section: Introductionmentioning

confidence: 99%

Retracted: MiR‐194‐5p inhibited metastasis and EMT of nephroblastoma cells through targeting Crk

Liu

Ren

Qü

et al. 2019

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

show abstract

“…CREB-induced LINC00473 acts as an oncogene in LKB1-inactivation NSCLC, CRTC1-MAML2 fusionpositive MEC, and several other cancer cells [18,19,[22][23][24]. In this work, we found that LINC00473 functioned as an oncogene in MCF-7 cells as well and discovered dual regulatory mechanisms of LINC00473 on CCND1 transcriptional control.…”

Section: Discussionmentioning

confidence: 52%

LINC00473 mediates cyclin D1 expression through a balance between activation and repression signals in breast cancer cells

Shi

Wang

2019

FEBS Letters

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) are critical regulators in tumorigenesis. However, their roles in breast cancer remain unclear. Here, we found that lncRNA LINC00473 is significantly upregulated in breast cancer cells. Loss‐ or gain‐of‐function experiments show that LINC00473 promotes cell proliferation. Mechanistically, LINC00473 is required for the activation of cyclin D1 (CCND1) expression through recruitment of phosphorylated CREB and histone acetylation to the CCND1 promoter. Interestingly, we found that LINC00473 is also required for maintaining the expression levels of the noncoding RNACCND1s and recruiting corepressor FUS to the CCND1 promoter. Altogether, the activation effect of LINC00473 on CCND1 is a net effect of two antagonistic regulatory pathways. Our finding provides a novel lncRNA‐mediated precise transcriptional control of CCND1.

show abstract

“…Increasing studies have certified that miRNAs are promising biomarkers for Wilms’ tumor treatment. For example, miR‐195 functioned as a tumor suppressor to regulate the progression of Wilms’ tumor by targeting IKKα (Zhu et al, 2018). miRNA‐572 facilitates metastasis and EMT process in Wilms’ tumor via targeting CDH1 (Zhang, et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

LINC00667 promotes Wilms’ tumor metastasis and stemness by sponging miR‐200b/c/429 family to regulate IKK‐β

Liu

Chen

Huang

et al. 2020

Cell Biology International

View full text Add to dashboard Cite

Wilms' tumor, also known as nephroblastoma, is a kind of pediatric renal cancer. Previous studies have indicated that microRNAs (miRNAs) regulate various cancers progression. However, whether miR-200 family regulated Wilms' tumor progression remains to be elucidated. In our study, miR-200b/c/429 expression was downregulated in Wilms' tumor tissue samples from 25 patients. And data from three independent analyses of quantitative real-time polymerase chain reaction revealed that the expression of miR-200b/c/429 was downregulated in Wilms' tumor cell lines. Functionally, Cell counting kit-8 assay revealed that cell viability was reduced by overexpressing miR-200b/c/429. Transwell assay manifested that cell migration and invasion was hindered by miR-200b/c/429 overexpression. Sphere-forming and western blot assays demonstrated that miR-200b/c/429 overexpression suppressed the sphere formation ability. Mechanically, nuclear factor-κB (NF-κB) pathway was confirmed to be associated with Wilms' tumor progression; miR-200b/c/429 overexpression inactivated NF-κB pathway as miR-200b/c/429 was identified to target IκB kinase β (IKK-β), an NF-κB pathway-related gene. Moreover, miR-200b/c/429 was sponged by LINC00667 in Wilms' tumor cells. LINC00667 competitively bound with miR-200b/c/429 to regulate IKK-β expression and then activated NF-κB pathway in Wilms' tumor. Subsequently, rescue assays illustrated that silencing of IKK-β could reverse the effect of miR-200b/c/429 inhibition on the progression of sh-LINC00667-transfected Wilms' tumor cells. In summary, LINC00667 promoted Wilms' tumor progression by sponging miR-200b/c/429 family to regulate IKK-β.

show abstract

LINC00473 antagonizes the tumour suppressor miR‐195 to mediate the pathogenesis of Wilms tumour via IKKα

Cited by 74 publications

References 28 publications

Retracted: MiR‐194‐5p inhibited metastasis and EMT of nephroblastoma cells through targeting Crk

Retracted: MiR‐194‐5p inhibited metastasis and EMT of nephroblastoma cells through targeting Crk

LINC00473 mediates cyclin D1 expression through a balance between activation and repression signals in breast cancer cells

LINC00667 promotes Wilms’ tumor metastasis and stemness by sponging miR‐200b/c/429 family to regulate IKK‐β

Contact Info

Product

Resources

About