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miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4
Yang, Miao,Liu, Ran,Li, Xiajun,Liao, Juan,Pu, Yuepu,Pan, Enchun,Yin, Lihong,Wang, Yi Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.12
In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA micro-array was applied to determine the genes that were regulated directly or indirectly by miR-183. 3'UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreover, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis further confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.
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Yunhui Li,Minhui Zhang,Xiaobo Li,Juan Zhang,Ran Liu,Geyu Liang,Yuepu Pu,Lihong Yin 대한독성 유전단백체 학회 2015 Molecular & cellular toxicology Vol.11 No.2
Caenorhabditis elegans (C. elegans), with homologous genes and conservative spermiogenesis in mammals, has a series of advantages to illuminate and study many biological processes including reproductive toxicity. So it is a very useful model to assess environmental and ecological toxicity. Here we introduce C. elegans as an animal model and three known mammalian sperm teratogens methyl methanesulfonate, mitomycin C and cyclophosphamide as experimental materials to elucidate the efficient and reliability for the assessment of chemicals altering spermiogenesis. The results showed that, with the aid of the brood size, spermatids activation, trans-activation, sperm competition as the endpoints, the adverse effects of three teratogens on C. elegans were detected. Thus, while the data of chemicals induced spermiogenesis abnormality is incomplete, we speculated that C. elegans could be a useful animal model to explore the effects on spermiogenesis of chemicals. And we propose an increased application of C. elegans that complements other model system in the reproductive toxicity.
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miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4
Miao Yang,Ran Liu,Xiajun Li,Juan Liao,Yuepu Pu,Enchun Pan,Lihong Yin,Yi Wang 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.12
In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA microarray was applied to determine the genes that were regulated directly or indirectly by miR-183. 3UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreo-ver, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis fur-ther confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.
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