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《miR - 29家族TET1的负反馈参与肝细胞癌》勘误

Erratum to: Negative feedback of miR-29 family TET1 involves in hepatocellular cancer.

作者信息

Lin Li Li, Wang Wei, Hu ZhaoYang, Wang Li Wen, Chang Jing, Qian HanGuang

机构信息

Department of Pharmacology, Wuxi Higher Health Vocational Technology School, No. 305, Xinguang Road, Wuxi, 214028, China.

出版信息

Med Oncol. 2015 Mar;32(3):39. doi: 10.1007/s12032-014-0437-2.

Abstract

Primary hepatocellular carcinoma (HCC) is the most common form of liver cancer and is one of the most common malignancies worldwide. Tumor suppressor gene silencing through DNA methylation contributes to cancer formation. The ten-eleven translocations (TET) family of α-ketogluta-rate-dependent dioxygenases catalyzes the sequential oxidation of 5-methylcytosine to 5-hydroxymethyl-cytosine, 5-formylcytosine and 5-carboxylcytosine, leading to eventual DNA demethylation. MicroRNAs are an abundant class of 17-25 nucleotides small noncoding RNAs, identified as important regulators of many diverse biological processes. In this study, we showed that TET1 expression was obviously reduced in the majority of examined HCC tissues. And we further investigated the expression and functional involvement of TET1 in proliferation, migration and invasion and determined that TET1 may function as a tumor suppressor. miR-29b was proved to inhibit metastasis through the targeting of TET1, indicating that downregulation of miR-29 may involve in HCC carcinogenesis and progression through potentiation of TET1 expression. Thus, we elucidated the roles of feedback of miR-29-TET1 downregulation in HCC development and suggested a potential target in identification of the prognosis and application of cancer therapy for HCC patients.

摘要

原发性肝细胞癌(HCC)是最常见的肝癌形式,也是全球最常见的恶性肿瘤之一。通过DNA甲基化导致的肿瘤抑制基因沉默促进癌症形成。α-酮戊二酸依赖性双加氧酶的十一易位(TET)家族催化5-甲基胞嘧啶依次氧化为5-羟甲基胞嘧啶、5-甲酰基胞嘧啶和5-羧基胞嘧啶,最终导致DNA去甲基化。微小RNA是一类丰富的17 - 25个核苷酸的小非编码RNA,被确定为许多不同生物过程的重要调节因子。在本研究中,我们发现大多数检测的HCC组织中TET1表达明显降低。我们进一步研究了TET1在增殖、迁移和侵袭中的表达及功能参与情况,并确定TET1可能作为一种肿瘤抑制因子发挥作用。已证明miR - 29b通过靶向TET1抑制转移,这表明miR - 29的下调可能通过增强TET1表达参与HCC的发生和进展。因此,我们阐明了miR - 29 - TET1下调反馈在HCC发展中的作用,并提出了一个在识别HCC患者预后和癌症治疗应用中的潜在靶点。

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