Expression profiling of micro-RNAs in human esophageal squamous cell carcinoma using RT-PCR

Ogawa, Ryo; Ishiguro, Hideyuki; Kuwabara, Yoshiyuki; Kimura, Masahiro; Mitsui, Akira; Katada, Takeyasu; Harata, Koshiro; Tanaka, Tatsuya; Fujii, Yoshitaka

doi:10.1007/s00795-009-0443-1

Cited by 101 publications

(81 citation statements)

References 24 publications

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“…Compared with NEST, a significant down-regulation of miR-210 expression was noted in ESCC. On the other hand, the expression of miR-31, which has been reported to be not altered between ESCC and NEST (16,17), showed no significant difference (Fig. 1B).…”

Section: Mir-210 Expression Is Significantly Down-regulated In Escc mentioning

confidence: 77%

MicroRNA-210 Regulates Cancer Cell Proliferation through Targeting Fibroblast Growth Factor Receptor-like 1 (FGFRL1)

Tsuchiya

Fujiwara

Sato

et al. 2011

Journal of Biological Chemistry

178

155

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The importance of microRNAs (miRNAs) in human malignancies has been well recognized. Here, we report that the expression of microRNA-210 (miR-210) is down-regulated in human esophageal squamous cell carcinoma and derived cell lines. Marked decreases in the level of miR-210 were observed especially in poorly differentiated carcinomas. We found that miR-210 inhibits cancer cell survival and proliferation by inducing cell death and cell cycle arrest in G 1 /G 0 and G 2 /M. Finally, we identified fibroblast growth factor receptor-like 1 (FGFRL1) as a target of miR-210 in esophageal squamous cell carcinoma and demonstrated that FGFRL1 accelerates cancer cell proliferation by preventing cell cycle arrest in G 1 /G 0 . Taken together, our findings show an important role for miR-210 as a tumor-suppressive microRNA with effects on cancer cell proliferation. MicroRNAs (miRNAs)2 are evolutionarily conserved small noncoding RNAs (20 -23 nucleotides) that bind to complementary sequences in the 3Ј-untranslated region (UTR) of target messenger RNAs (mRNAs) and regulate gene expression by the cleavage of target mRNAs and/or translational inhibition (1). Currently, Ͼ800 human miRNAs have been identified and registered in the miRNA database, miRBase (2). miRNAs play important roles in the differentiation of various cell types and in the initiation and progression of cancer, and it has been shown that the expression of some miRNAs is altered during cell differentiation and in malignancies (1, 3, 4).In a recent study, we identified microRNA-210 (miR-210) as one of the miRNAs that is markedly differentially expressed during the process of epithelial differentiation (3). It has been reported that miR-210 expression is down-regulated during epithelial-mesenchymal transition, the aberrant activation of which triggers cancer pathology (5). Carcinomas are derived from epithelial cells, and poor prognosis in patients with carcinoma is associated with the disruption of characteristics of differentiated epithelial cells, such as cell junctions and polarity (6 -8). Hence, given that the expression of miR-210 appears to be correlated well with epithelial differentiation, miR-210 might play a suppressive role in carcinomas. In support of this idea, allelic deletions at the miR-210 locus have been observed in 64% of cases of ovarian cancer (9), and ectopic expression of miR-210 represses tumor growth when human cancer cell lines are implanted into immunodeficient mice (10). However, the clinical roles of miR-210 in carcinomas and the mechanisms by which it represses tumor growth remain unknown.In this study, we investigated the functional role of miR-210 in the growth of carcinomas and the mechanism by which it acts using clinical samples as well as cell lines of esophageal squamous cell carcinoma (ESCC). ESCC is a highly aggressive malignancy with a 5-year survival rate of 10% worldwide. It has been used as a model to study the mechanisms of dysregulated epithelial differentiation and epithelial-mesenchymal transition in carcinomas (11, 12). E...

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Section: Mir-210 Expression Is Significantly Down-regulated In Escc mentioning

confidence: 77%

MicroRNA-210 Regulates Cancer Cell Proliferation through Targeting Fibroblast Growth Factor Receptor-like 1 (FGFRL1)

Tsuchiya

Fujiwara

Sato

et al. 2011

Journal of Biological Chemistry

178

155

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“…miR-132 expression has been reported to be increased in several types of cancers including lung cancer (14), squamous cell carcinoma of the tongue (23), colorectal carcinoma (24) and esophageal cancer (25). However, decreased miR-132 expression has been observed in osteosarcoma (26) and liver cancer (27).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells

et al. 2014

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Abstract. Lung cancer is the leading cause of cancer-related mortality worldwide. microRNAs (miRNAs) are small posttranscriptional regulatory non-coding RNAs that function as oncogenes or tumor suppressors in human cancers. Emerging evidence reveals that deregulation of miRNAs contributes to the progression of human lung cancer, which is the leading cause of cancer-related deaths worldwide. In the present study, we found that upregulation of the miR-212/132 cluster significantly suppressed the growth and focus formation of A549 and H1299 cells. Moreover, forced expression of this cluster conferred radiosensitivity and inhibited the migration of lung cancer cells, whereas downregulation of miR-212/132 reversed the above effects. Furthermore, miR-212/132 overexpression induced cell cycle arrest at the G1/S phase transition of the lung cancer cells, and inhibition of miR-132 and miR-212 abrogated this arrest. In addition, miR-212/132 overexpression increased the percentage of cells undergoing apoptosis. Cells transfected with the miR-212/132 cluster exhibited upregulated p21 expression and reduced cyclin D1 expression. Conversely, cells transfected with the miR-212/132 inhibitor showed reduced expression of p21 and upregulated expression of cyclin D1, suggesting that miR-212/132 may mediate proliferation and cell cycle arrest through p21 and cyclin D1. Our study provides insight into the biological function of the miR-212/132 cluster in lung cancer. The present study may provide a potential therapeutic target for the treatment of lung cancer.

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“…The global miRNA expression analyses (hierarchical clustering and principal component analysis) showed that the expression profiles of the miRNAs differed between the cisplatin-sensitive and -resistant cell lines (Figure 2), and expression levels of 45 miRNAs were changed by more than fourfold in cisplatin-sensitive cell lines as compared with cisplatin-resistant cell lines (Supplementary Table 1). Subsequently, the expression levels of the 10 miRNAs that were selected according to the miRNA microarray data and literature search [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39] were validated by quantitative reverse transcription-PCR. This confirmed that miR-141, miR-21, miR-19b, miR-200a, miR-19a, miR-27a, miR-20a and miR-20b were expressed at significantly higher levels in the cisplatinresistant lines, and miR-205 and miR-224 at significantly lower levels than in the cisplatin-sensitive cell lines (Po0.05) (Table 1).…”

Section: Cisplatin-sensitive and -Resistant Human Escc Cell Linesmentioning

confidence: 99%

MicroRNA-141 confers resistance to cisplatin-induced apoptosis by targeting YAP1 in human esophageal squamous cell carcinoma

et al. 2011

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MicroRNAs (miRNAs) are endogenous non-coding RNAs that function as negative regulators of gene expression. Alterations in miRNA expression have been shown to affect tumor growth and response to chemotherapy. In this study, we explored the possible role of miRNAs in cisplatin resistance in esophageal squamous cell carcinoma (ESCC). First we assessed the sensitivity of nine human ESCC cell lines (KYSE series) to cisplatin using an in vitro cell viability assay, and then we compared the miRNA profiles of the cisplatin-sensitive and -resistant cell lines by miRNA microarray analysis. The two groups showed markedly different miRNA expression profiles, and 10 miRNAs were found to be regulated differentially between the two groups. When miR-141, which was the most highly expressed miRNA in the cisplatin-resistant cell lines, was expressed ectopically in the cisplatin-sensitive cell lines, cell viability after cisplatin treatment was increased significantly. Furthermore, we found that miR-141 directly targeted the 3¢-untranslated region of YAP1, which is known to have a crucial role in apoptosis induced by DNA-damaging agents, and thus downregulated YAP1 expression. Our study highlights an important regulatory role for miR-141 in the development of cisplatin resistance in ESCC.

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Expression profiling of micro-RNAs in human esophageal squamous cell carcinoma using RT-PCR

Cited by 101 publications

References 24 publications

MicroRNA-210 Regulates Cancer Cell Proliferation through Targeting Fibroblast Growth Factor Receptor-like 1 (FGFRL1)

MicroRNA-210 Regulates Cancer Cell Proliferation through Targeting Fibroblast Growth Factor Receptor-like 1 (FGFRL1)

Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells

MicroRNA-141 confers resistance to cisplatin-induced apoptosis by targeting YAP1 in human esophageal squamous cell carcinoma

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