MiRNA‐26b regulates the expression of cyclooxygenase‐2 in desferrioxamine‐treated CNE cells

Ji, Yanhong; He, Yonghong; Liu, Le; Zhong, Xingyuan

doi:10.1016/j.febslet.2010.01.036

Cited by 56 publications

(51 citation statements)

References 33 publications

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“…It has been demonstrated that miR-26b and miR-16 regulate COX-2 expression in some cancer cells (Ji et al 2010;Young et al 2012). However, to our knowledge, so far, there is no insight into the relationship between COX-2 upregulation and altered miRNA profile in macrophages of senescence mice.…”

Section: Tsa Suppresses Cox-2 Protein Expression By Upregulation Of Mmentioning

confidence: 96%

“…3a, b, left). It has been reported that the two miRNAs are involved in the regulation of COX-2 expression in certain cell lines (Hao et al 2011;Ji et al 2010;Li et al 2013;Strillacci et al 2009). Therefore, we here focused on miR-101b and miR-26b expression in the mouse peritoneal macrophages.…”

Section: Lps Enhances Expression Of Cox-2 and Pge2 In Aged Mouse Perimentioning

confidence: 99%

“…COX-2 mRNA translation inhibition could be mediated by several miRNAs. For example, mmu-miR-101a and mmu-miR-199a* affect embryo implantation of mice by post-transcriptional regulation of COX-2 (Chakrabarty et al 2007) and miR26b could regulate the expression of COX-2 in desferrioxamine-treated CNE cells (Ji et al 2010).…”

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confidence: 99%

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Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

Liú

Wang

et al. 2015

AGE

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Aging is the natural process of decline in physiological structure and function of various molecules, cells, tissues, and organs. Growing evidence indicates that increased immune genetic diversity and dysfunction of immune system cause aging-related pathophysiological process with the growth of age. In the present study, we observed that LPS-induced higher activation of cyclooxygenase (COX)-2 promoter is associated with the upregulated binding activity of nuclear factor kappa B (NF-κB) in peritoneal macrophages of aged mice than young ones. Additionally, COX-2 is a direct target of miR-101b and miR-26b in the macrophages. Significant upregulation of miR-101b and miR26b effectively prevented LPS-induced excessive expression of COX-2 in the young mice. Because these negative regulatory factors were unresponsive to LPS stimulation, the levels of COX-2 were markedly higher in the macrophages of aged mice. Further study showed that NF-κB activation contributed to the increase in the expression of miR-101b and miR-26b in the LPSstimulated macrophages of young mice, but not aged ones. Moreover, histone deacetylase (HDAC) inhibitor trichostatin A (TSA) upregulated expression of miR101b and miR-26b in the aged mouse macrophages only, but not the young cells. This demonstrated that HDAC suppressed the expression of miR-101b and miR-26b in the LPS-treated macrophages of aged mice and contributed to the aging process. TSA-induced increased expression of miR-101b and miR-26b could further suppress COX-2 expression. These findings provide novel evidence on the regulation of immune senescence and miR-101b and miR-26b, which might be promising targets in treating aged-related inflammatory diseases. Epigenetic regulation of the microRNAs (miRNAs) provides an important evidence for the treatment of innate inflammatory disease with HDAC inhibitors in elderly.

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Section: Tsa Suppresses Cox-2 Protein Expression By Upregulation Of Mmentioning

confidence: 96%

Section: Lps Enhances Expression Of Cox-2 and Pge2 In Aged Mouse Perimentioning

confidence: 99%

See 1 more Smart Citation

Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

Liú

Wang

et al. 2015

AGE

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“…Growing evidence indicates that miR26 is downregulated in human cancers, including nasopharyngeal carcinoma (16), breast cancer (17,18), hepatocellular carcinoma (19), parathyroid tumors (20), rhabdomyosarcoma (21), and non-small cell lung cancer (22). In addition, ectopic expression of miR26b leads to apoptosis in cancer cells by targeting pRb5 (23) and PTGS2 (24).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

Zhang

Xiao

Wang

et al. 2014

Molecular Cancer Research

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Cancer is characterized by mutations, genome rearrangements, epigenetic changes, and altered gene expression that enhance cell proliferation, invasion, and metastasis. To accommodate deregulated cellular proliferation, many DNA replication-initiation proteins are overexpressed in human cancers. However, the mechanism that represses the expression of these proteins in normal cells and the cellular changes that result in their overexpression are largely unknown. One possible mechanism is through miRNA expression differences. Here, it is demonstrated that miR26a and miR26b inhibit replication licensing and the proliferation, migration, and invasion of lung cancer cells by targeting CDC6. Importantly, miR26a/b expression is significantly decreased in human lung cancer tissue specimens compared with the paired adjacent normal tissues, and miR26a/b downregulation and the consequential upregulation of CDC6 are associated with poorer prognosis of patients with lung cancer. These results indicate that miR26a/b repress replication licensing and tumorigenesis by targeting CDC6. Implications:The current study suggests that miR26a, miR26b, and CDC6 and factors regulating their expression represent potential cancer diagnostic and prognostic markers as well as anticancer targets.

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“…miRNAs may regulate the expression of related target genes to participate in cell differentiation, proliferation, apoptosis, tumor invasion and metastasis, and stem cell regulation (Hammond, 2007;Yu et al, 2010;Pizzini et al, 2013;Zhang et al, 2013). miRNA-26b is an miRNA that plays a role as a tumor suppressor gene or oncogene in different tumors, such as lung cancer, breast cancer, bladder cancer, and liver cancer (Ji et al, 2009;Ji et al, 2010;Gao et al, 2011;Liu et al, 2011;Palumbo et al, 2013). However, few studies have investigated its role in the occurrence and development of osteosarcoma.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-26b inhibits osteosarcoma cell migration and invasion by down-regulating PFKFB3 expression

2015

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MiRNA‐26b regulates the expression of cyclooxygenase‐2 in desferrioxamine‐treated CNE cells

Cited by 56 publications

References 33 publications

Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

Dysregulated expression of miR-101b and miR-26b lead to age-associated increase in LPS-induced COX-2 expression in murine macrophage

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

MicroRNA-26b inhibits osteosarcoma cell migration and invasion by down-regulating PFKFB3 expression

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