MiR-101 downregulation is involved in cyclooxygenase-2 overexpression in human colon cancer cells

Strillacci, Antonio; Griffoni, Cristiana; Sansone, Pasquale; Paterini, Paola; Piazzi, Giulia; Lazzarini, Giorgia; Spisni, Enzo; Pantaleo, Maria Abbondanza; Biasco, Guido; Tomasi, Vittorio

doi:10.1016/j.yexcr.2008.12.010

Cited by 216 publications

(186 citation statements)

References 40 publications

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“…As an aspect of the relationship with the microRNA-101, the prediction based on PicTar and TargetScan DNA analysis software suggest that COX-2 could be one direct target for miR-101 because miR-101 has a seed region, which is able to bind to the COX-2 mRNA 3-UTR. Such as miR-101 and COX-2 can control the development of mammary gland (Tanaka et al, 2009), colon cancer (Strillacci et al 2009) and prostate cancer (Hao et al, 2011). In recent years, studies have found that some cancer cells ,which have a high-expression of COX-2, their ability of the proliferation and metastasis have also been highly focused.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-101 Inhibits Cell Proliferation, Invasion, and Promotes Apoptosis by Regulating Cyclooxygenase-2 in Hela Cervical Carcinoma Cells

Huang¹,

Chen²,

Shi³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

MicroRNA-101 Inhibits Cell Proliferation, Invasion, and Promotes Apoptosis by Regulating Cyclooxygenase-2 in Hela Cervical Carcinoma Cells

Huang¹,

Chen²,

Shi³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…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%

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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“…miR-101 has multiple predicted targets, such as Cox-2, Mcl-1 and FOS. These genes have been confirmed as targets of miR-101 by the luciferase reporter assay (32,33,35). This evidence suggests that miR-101 modulates multiple steps, such as proliferation, adhesion and migration of tumor cells, in lung cancer.…”

Section: A B Cmentioning

confidence: 75%

microRNA-101 inhibits lung cancer invasion through the regulation of enhancer of zeste homolog 2

Cho

Jeon

Lee

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. microRNAs (miRNAs) may function as oncogenes or tumor-suppressor genes depending on the targets that are regulated. Enhancer of zeste homolog 2 (EZH2) is the target of miR-101 and a member of the polycomb repressive complex 2, which is involved in the methylation of histone H3 at lysine 27 (H3K27). Therefore, we aimed to ascertain whether or not the overexpression of miR-101 inhibits invasion of lung cancer through regulation of EZH2. In this study, the expression of miR-101 was down-regulated and the expression of EZH2 was up-regulated in lung cancer. Global methylation of H3K27 was higher in metastatic lung cancer than in early lung cancer lesions. Overexpression of miR-101 induced a marked reduction in EZH2 mRNA levels in several lung cancer cell lines. A reduction in the trimethyl H3K27 histone mark was detected at the CDH1 promoter in miR-101 precursor-transfected cells. Moreover, the expression of CDH1 and MMP-2 was reversed by miR-101 transfection. Therefore, the overexpression of miR-101 inhibits the invasiveness of lung cancer. miR-101 may be a potent tumor suppressor by altering chromatin structure through repression of EZH2 and may be a potential therapeutic tool for patients with lung cancer.

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MiR-101 downregulation is involved in cyclooxygenase-2 overexpression in human colon cancer cells

Cited by 216 publications

References 40 publications

MicroRNA-101 Inhibits Cell Proliferation, Invasion, and Promotes Apoptosis by Regulating Cyclooxygenase-2 in Hela Cervical Carcinoma Cells

MicroRNA-101 Inhibits Cell Proliferation, Invasion, and Promotes Apoptosis by Regulating Cyclooxygenase-2 in Hela Cervical Carcinoma Cells

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

microRNA-101 inhibits lung cancer invasion through the regulation of enhancer of zeste homolog 2

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