miR-186, miR-216b, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting α subunit of protein kinase CKII in human colorectal cancer cells

Kim, Soo Young; Lee, Younghoon; Bae, Young‐Seuk

doi:10.1016/j.bbrc.2012.10.117

Cited by 98 publications

(74 citation statements)

References 27 publications

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“…S2D). Recently, 4 miRNAs, including miR-760, have been reported to cooperatively induce cellular senescence by targeting a subunit of protein kinase CKII in human colorectal cancer cells (23). Our in silico analysis also indicated that several miRNAs, including miR-760, targeted histone mRNAs cooperatively.…”

Section: Discussionsupporting

confidence: 57%

Contrasting Expression Patterns of Histone mRNA and microRNA 760 in Patients with Gastric Cancer

Iwaya

Fukagawa

Suzuki

et al. 2013

Clinical Cancer Research

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Purpose: Recent studies revealed that both disseminated tumor cells and noncancerous cells contributed to cancer progression cooperatively in the bone marrow. Here, RNA-seq analysis of bone marrow from gastric cancer patients was performed to identify prognostic markers for gastric cancer.Experimental Design: Bone marrow samples from eight gastric cancer patients (stages I and IV: n ¼ 4 each) were used for RNA-seq analysis. Results were validated through quantitative real-time PCR (qRT-PCR) analysis of HIST1H3D expression in 175 bone marrow, 92 peripheral blood, and 115 primary tumor samples from gastric cancer patients. miR-760 expression was assayed using qRT-PCR in 105 bone marrow and 96 primary tumor samples. Luciferase reporter assays were performed to confirm whether histone mRNAs were direct targets of miR-760. miR-760 expression was also evaluated in noncancerous cells from gastric cancer patients.

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Section: Discussionsupporting

confidence: 57%

Contrasting Expression Patterns of Histone mRNA and microRNA 760 in Patients with Gastric Cancer

Iwaya

Fukagawa

Suzuki

et al. 2013

Clinical Cancer Research

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“…This observation further confirms miR-186 is an important regulator of cell cycle progression. Moreover, miR-186 downregulates the expression of CKIIa, of which downregulation induces cellular senescence in human colon cancer HCT116 cells (Kim et al, 2012). These observations suggest that miR-186 negatively regulates cell growth through cell cycle arrest and apoptosis, at least in tumor cells and fibroblasts.…”

Section: Discussionmentioning

confidence: 82%

“…Moreover, miR-186 stimulates degradation of CKIIa mRNA by targeting its 3' untranslated regions (UTRs). Downregulation of protein kinase CKII induces cellular senescence in human colon cancer HCT116 cells (Kim et al, 2012). The miR-186 mimics increased senescent-associated β-galactosidase (SA-β-gal) staining, p53 and p21Cip1/WAF1 expression, and reactive oxygen species (ROS) production.…”

Section: Introductionmentioning

confidence: 99%

miR-186 Regulates Glycolysis through Glut1 During the Formation of Cancer-associated Fibroblasts

Sun¹,

Hu²,

Xiong³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Emerging evidence has suggested that glycolysis is enhanced in cancer-associated fibroblasts (CAF), and miR-186 is downregulated during the CAF formation. However, it is not clear whether miR-186 is involved in the regulation of glycolysis and what the role of miR-186 plays during the CAF formation. In this study, quantitative PCR analysises show miR-186 is downregulated during the CAF formation. Moreover, miR-186 targets the 3' UTR of Glut1, and its overexpression results in the degradation of Glut1 mRNA, which eventually reduces the level of Glut1 protein. On the other hand, knockdown of miR-186 increased the expression of Glut1. Both time course and dose response experiments also demonstrated that the protein and mRNA levels of Glut1 increase during CAF formation, according to Western blot and quantitative PCR analyses, respectively. Most importantly, besides the regulation on cell cycle progression, miR-186 regulates glucose uptake and lactate production which is mediated by Glut1. These observations suggest that miR-186 plays important roles in glycolysis regulation as well as cell cycle checkpoint activation.

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“…Both in vitro and in vivo assays revealed that miR-216b attenuates cell proliferation, invasion and tumor growth in nude mice (74). In addition, miR-216b, miR-186, miR-337-3p and miR-760 were found to cooperatively promote cellular senescence through the p53-p21 (Cip1/ WAF1) pathway in human colorectal cancer cells (75). Given that the overexpression of miR-486-5p is closely correlated with the downregulated expression of ARHGAP5 in lung tumor tissues, which considerably inhibits lung cancer cell migration and invasion, miR-486-5p may act as a tumor suppressor contributing to the progression and metastasis of non-small cell lung cancer (76).…”

Section: Microrna-mrna Prediction Tool ------------------------------mentioning

confidence: 98%

Upregulation of NEK2 is associated with drug resistance in ovarian cancer

et al. 2013

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Abstract. NEK2 [NIMA (never in mitosis gene A)-related expressed kinase 2] is associated with various biological behaviors in the development of cancer, while research concerning its association with drug resistance is limited. The association of NEK2 with drug resistance in ovarian cancer has not yet been reported. In the present study, on the basis of microarray results from Oncomine and the GEO Profiles online database, we revealed that NEK2 mRNA expression in ovarian cancer tissues is upregulated. In addition, its expression in drugresistant ovarian cancer cells was upregulated when compared with expression with their sensitive or parental counterparts. Finally, we performed a comprehensive bioinformatic analysis consisting of protein/gene-protein/gene interaction network, annotation of biological processes and microRNA-mRNA interaction analysis. We observed that NEK2 directly or indirectly interacts with a number of genes, proteins, microRNAs and biological processes associated with drug resistance in ovarian and other types of cancer. These results indicate that NEK2 contributes to drug resistance in ovarian cancer and it may be an important therapeutic target.

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miR-186, miR-216b, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting α subunit of protein kinase CKII in human colorectal cancer cells

Cited by 98 publications

References 27 publications

Contrasting Expression Patterns of Histone mRNA and microRNA 760 in Patients with Gastric Cancer

Contrasting Expression Patterns of Histone mRNA and microRNA 760 in Patients with Gastric Cancer

miR-186 Regulates Glycolysis through Glut1 During the Formation of Cancer-associated Fibroblasts

Upregulation of NEK2 is associated with drug resistance in ovarian cancer

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