MicroRNA‐26‐5p functions as a new inhibitor of hepatoblastoma by repressing lin‐28 homolog B and aurora kinase a expression

Zhang, Yutong; Zhao, Yulan; Wu, Jiang; Liangpunsakul, Suthat; Niu, Junqi; Wang, Li

doi:10.1002/hep4.1185

Cited by 20 publications

(16 citation statements)

References 34 publications

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“…Like in hepatoblastoma, AML and multiple myeloma, in this study, miR‐26a‐5p was also found downregulated in breast cancer, and low expression of miR‐26a‐5p predicted a negative index for the overall survival of breast cancer patients (Figure ). Overexpression of miR‐26a‐5p markedly inhibited breast cancer cell growth, and decreased the expression levels of cell cycle‐associated proteins (Figure ), which suggested that miR‐26a‐5p was a potential biomarker for breast cancer.…”

Section: Discussionsupporting

confidence: 57%

“…MiR‐26a‐5p has been reported to be involved in the pathogenesis of several tumors. A recent paper reported that miR‐26a‐5p was a newly identified repressor of hepatoblastoma cell growth, and the decreased miR‐26a‐5p expression was correlated with the poor outcome of patients with hepatoblastoma . MiR‐26a‐5p targeted the 3′‐untranslated regions of LIN28B and AURKA, and markedly inhibited their expressions, along with suppressing hepatoblastoma cell growth and clonality .…”

Section: Introductionmentioning

confidence: 99%

“…A recent paper reported that miR‐26a‐5p was a newly identified repressor of hepatoblastoma cell growth, and the decreased miR‐26a‐5p expression was correlated with the poor outcome of patients with hepatoblastoma . MiR‐26a‐5p targeted the 3′‐untranslated regions of LIN28B and AURKA, and markedly inhibited their expressions, along with suppressing hepatoblastoma cell growth and clonality . In acute myeloid leukemia (AML), miR‐26a‐5p was found downregulated by a miRNA expression assay, and peroxiredoxin III (PrxIII) was identified as a direct target of miR‐26a‐5p .…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐26a‐5p inhibits breast cancer cell growth by suppressing RNF6 expression

Huang

Yang

et al. 2019

The Kaohsiung J of Med Scie

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MicroRNA-26a-5p (miR-26a-5p) has been reported to be involved in the tumorigenesis of several tumors, but its function in breast cancer is still unknown. In this study, miR-26a-5p was found significantly downregulated in both of the breast cancer tissues and cell lines, and low expression of miR-26a-5p predicted a poor prognosis for breast cancer patients. Overexpression of miR-26a-5p could significantly inhibit breast cancer cell growth. Further studies revealed that overexpression of miR-26a-5p downregulated the protein levels of Cyclin D1, CDK4, and CDK6, but upregulated the expression levels of p21, p27, and p53. In mechanism, miR-26a-5p targeted the 3 0 UTR of ring finger protein 6 (RNF6) mRNA and inhibited RNF6 expression in breast cancer cells.Moreover, overexpression of miR-26a-5p inhibited RNF6/ERα/Bcl-xL axis in breast cancer cells. In contrast, inhibiting miR-26a-5p upregulated RNF6/ERα/Bcl-xL axis.Further studies indicated that miR-26a-5p mediated RNF6/ERα/Bcl-xL axis through regulating the stability of ERα protein. Collectively, downregulation of miR-26a-5p plays essential roles in breast cancer by mediating RNF6/ERα/Bcl-xL axis, which might provide important implications for the therapeutics of breast cancer.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐26a‐5p inhibits breast cancer cell growth by suppressing RNF6 expression

Huang

Yang

et al. 2019

The Kaohsiung J of Med Scie

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“…Recently, Zhang et al . showed in hepatoblastoma cells that miRNA‐26‐5p inhibited cell growth and proliferation by targeting LIN28B and aurora kinase A . In the present study, for the first time we showed that ALR induced proliferation through upregulation of miRNA‐26a, targeting the downregulation of PTEN, resulting in an enhanced p‐Akt/cyclin D1 pathway in hepatic cells.…”

Section: Introductionsupporting

confidence: 59%

Augmenter of liver regeneration enhances cell proliferation through the microRNA‐26a/Akt/cyclin D1 pathway in hepatic cells

Gupta

Sata

Ahamad

et al. 2019

Hepatology Research

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Aim Hepatocytes can proliferate and regenerate when injured by toxins, viral infections, and so on. Augmenter of liver regeneration (ALR) is a key regulator of liver regeneration, but the mechanism is unknown. The role of ALR in other cell types is not known. In the present study, we investigated the relationship between microRNA (miRNA)‐26a and ALR in the Huh7 cell line and adipose tissue‐derived mesenchymal cells from chronic liver disease patients and healthy individuals. Methods Huh7 cells were transfected independently with ALR and miRNA‐26a expression vectors, and their effects on cell proliferation, the expression of miRNA‐26a, and activation of the phosphatase and tensin homolog and Akt signaling pathways were determined. The experiments were repeated on mesenchymal stem cells derived from healthy individuals and chronic liver disease patients to see whether the observations can be replicated in primary cells. Results Overexpression of ALR or miRNA‐26a resulted in an increase of the phosphorylation of Akt and cyclin D1 expression, whereas it resulted in decreased levels of p‐GSK‐3β and phosphatase and tensin homolog in Huh7 cells. The inhibition of ALR expression by ALR siRNA or anti‐miR‐26a decreased the Akt/cyclin D1 signaling pathway, leading to decreased proliferation. Mesenchymal stem cells isolated from the chronic liver disease patients had a higher ALR expression, while the mesenchymal stem cells isolated from healthy volunteers responded to the growth factor treatments for increased ALR expression. It was found that there was a significant increase in miRNA‐26a expression and proliferation. Conclusions These data clearly showed that ALR induced the expression of miRNA‐26a, which downregulated phosphatase and tensin homolog, resulting in an increased p‐Akt/cyclin D1 pathway and enhanced proliferation in hepatic cells.

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“…It is noteworthy that two of the miRNAs (miR-125b and let-7a) in the cluster are LIN28B-related miRNA [27], indicating a potential molecular mechanism. Meanwhile, LIN28B and AURKA expressions were upregulated in a transcriptomic and genomic analysis of human hepatoblastoma, and miRNA-26-5p inhibited hepatoblastoma by repressing LIN28B [44]. LIN28B might also increase the risk of hepatoblastoma through LIN28B-RAN-AURKA pathway [44].…”

Section: Discussionmentioning

confidence: 98%

LIN28B gene polymorphisms modify hepatoblastoma susceptibility in Chinese children

et al. 2020

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Hepatoblastoma is one of the malignant liver tumors in children. However, genetic mechanisms underpinning the initiation of hepatoblastoma remain largely unclear. The previous study showed that lin-28 homolog B (LIN28B) might play a role in the development of hepatoblastoma. To detect the association between LIN28B gene polymorphisms and hepatoblastoma risk in Chinese children, we conducted a five-center case-control study of 275 hepatoblastoma patients and 1018 cancer-free controls. Four potentially functional polymorphisms were genotyped using the Taqman method. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate the strength of the associations. We found that the rs314276 C>A polymorphism (AA vs. CC: adjusted OR=2.05, 95% CI=1.36-3.10, P=0.0006; AA vs. CA/CC: adjusted OR=2.11, 95% CI=1.43-3.12, P=0.0002) and rs9404590 T>G (GG vs. TT: adjusted OR=1.89, 95% CI=1.20-3.00, P=0.007; GG vs. TT/TG: adjusted OR=1.87, 95% CI=1.20-2.92, P=0.006) were associated with increased hepatoblastoma risk. Combination analysis of risk genotypes showed that patients with four risk genotypes had a higher chance of developing hepatoblastoma than carriers of 1 to 3 risk genotypes. Stratification analysis showed the significant association between the rs314276 AA genotype and hepatoblastoma risk in both age and sex groups, as well as clinical stages III+IV cases. The rs9404590 GG genotype was associated with hepatoblastoma risk in participants' ≥17 months, in females, and for those with clinical stages III+IV disease. Furthermore, four risk genotypes confer higher hepatoblastoma susceptibility in both age and sex groups, as well as groups with clinical stages III+IV disease. Genotype-based gene expression analysis confirmed that the rs9404590 T>G polymorphism was significantly associated with altered LIN28B gene expression. We further validated our findings using false-positive probability analysis. This finding suggested that LIN28B gene polymorphisms may be associated with an increased predisposition to hepatoblastoma.

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MicroRNA‐26‐5p functions as a new inhibitor of hepatoblastoma by repressing lin‐28 homolog B and aurora kinase a expression

Cited by 20 publications

References 34 publications

MicroRNA‐26a‐5p inhibits breast cancer cell growth by suppressing RNF6 expression

MicroRNA‐26a‐5p inhibits breast cancer cell growth by suppressing RNF6 expression

Augmenter of liver regeneration enhances cell proliferation through the microRNA‐26a/Akt/cyclin D1 pathway in hepatic cells

LIN28B gene polymorphisms modify hepatoblastoma susceptibility in Chinese children

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