MiR-200 family and cancer: From a meta-analysis view

Huang, Guoliang; Sun, Jiancong; Lü, Yan; Liu, Yuke; Cao, Huiyuan; Zhang, Huanyu; Calin, George A.

doi:10.1016/j.mam.2019.09.005

Cited by 56 publications

(50 citation statements)

References 94 publications

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“…In colon cancer, an increasing number of studies have shown that various miRNAs are involved in the process of colon cancer, including miR-200c [5,6]. The expression of miR-200c has been found to correlate with poor prognosis of colon cancer [6].The miR-200 family comprises 5 members, miR-200a/b/429 and miR-200c/141 [7]. Accumulating evidence suggests that miR-200c, a tumour suppressor, has low expression in colon cancer [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

Cong

Yang

Xia

et al. 2020

Preprint

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BackgroundMicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer.MethodsThe miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed.ResultsIn vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study.ConclusionsIn summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

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Section: Introductionmentioning

confidence: 99%

The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

Cong

Yang

Xia

et al. 2020

Preprint

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“…MiR‐140‐5p inhibits Wilms’ tumor proliferation via targeting TGFBRI/SMAD2/3 and IGF‐1R/AKT signaling pathways (Liu et al, 2019). A recent literature has highlighted the significant association between miR‐200 family and prognosis of various cancer types (Huang et al, 2019). However, the function of miR‐200 family in Wilms’ tumor was largely unknown.…”

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

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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.

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“…The miR-200 family comprises 5 members which located in miR-200a/b/429 and miR-200c/141. 8 Accumulating evidence suggests that miR-200 family is an epigenetic regulator of epithelialto-mesenchymal transition and involved in cancer progression. 9,10 Among them, there are many studies on miR-200c and colon cancer, and it has been shown that low expression of miR-200c is associated with poor prognosis of patients.…”

Section: Introductionmentioning

confidence: 99%

miR-200c /FUT4 axis prevents the migration, invasion and proliferation of colon cancer cells by downregulating Wnt/β-catenin pathway

Cong

Yang

Xia

et al. 2020

Preprint

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Background To investigate the effects of miR-200c targeting fucosyltransferase 4 (FUT4) on the proliferation, migration and invasion of colon cancer cells and further to explore its mechanism. Methods The expression of miR-200c and FUT4 mRNA in Lovo and SW480 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analyzed by Pearson. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into Lovo and SW480 cells, and RT-PCR was used to analyze the effect of transfection. Cell counting kitcck-8 (CCK-8), cloning and transwell assays were used to detect the migration, invasion and proliferation of Lovo and SW480 cells, respectively. Immunofluorescence was used to analyze the expression of Ki-67 protein. Moreover, the expression of Wnt/β-catenin signaling pathway-related proteins were detected by western blot. Double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. Results Pearson results showed that miR-200c and FUT4 were negatively correlated in Lovo and SW480 cells (correlation coefficients were − 0.9046 and − 0.9236, respectively). MiR-200c overexpression inhibits the proliferation, migration and invasion of Lovo cells by down-regulating FUT4. The expression of Ki67 positive cells and Wnt/β-catenin signaling pathway-related proteins were reduced in miR-200c overexpression and FUT4 silencing groups. The scientific search and dual luciferase reporting system identified FUT4 was the target of miR-200c. Conclusion In conclusion, miR-200c overexpression inhibits FUT4 expression and down-regulates the Wnt/β-catenin signaling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

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MiR-200 family and cancer: From a meta-analysis view

Cited by 56 publications

References 94 publications

The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

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

miR-200c /FUT4 axis prevents the migration, invasion and proliferation of colon cancer cells by downregulating Wnt/β-catenin pathway

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