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微 RNA-132 在乳腺导管原位癌 (DCIS) 中经常下调,通过抑制细胞增殖发挥肿瘤抑制作用。

MicroRNA-132 is frequently down-regulated in ductal carcinoma in situ (DCIS) of breast and acts as a tumor suppressor by inhibiting cell proliferation.

机构信息

Department of Breast Cancer Pathology and Research Laboratory, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, PR China.

出版信息

Pathol Res Pract. 2013 Mar;209(3):179-83. doi: 10.1016/j.prp.2012.12.002. Epub 2013 Feb 8.

Abstract

Ductal carcinoma in situ (DCIS) is the most common type of non-invasive breast cancer. The currently accepted step-wise model suggests that breast cancer progressed in the following manner: normal breast cell→usually ductal hyperplasia (UDH)→atypical ductal hyperplasia (ADH)→DCIS→invasive ductal carcinoma (IDC). Therefore, DCIS can serve as a good model to analyze the mechanism underlying invasive breast cancer occurrence. MicroRNAs (miRNAs) are a novel class of small non-coding RNAs (~22nt) involved in the regulation of various biological processes. Altered miRNA expression could also contribute to the origination of cancer, including breast cancer. Here, by using miRNA microarray and real time PCR, we analyzed the miRNA expression profile in 21 DCIS and the corresponding normal tissues. miR-10b, miR-125b, miR-132, miR-145, miR-154-3p, miR-382-5p and miR-409-3p were found to be significantly deregulated in DCIS. Results from CCK-8 assay showed that the overexpression of miR-132 could inhibit the proliferation of breast cancer cell line. High expression of miR-132 could also inhibit the colony formation. Our findings will lead to further understanding of the development of breast cancer.

摘要

导管原位癌(DCIS)是最常见的非浸润性乳腺癌类型。目前公认的逐步模型表明,乳腺癌的进展方式如下:正常乳腺细胞→通常是导管增生(UDH)→非典型导管增生(ADH)→DCIS→浸润性导管癌(IDC)。因此,DCIS 可以作为分析浸润性乳腺癌发生机制的良好模型。microRNAs(miRNAs)是一类新型的小非编码 RNA(~22nt),参与调节各种生物学过程。miRNA 表达的改变也可能导致癌症的发生,包括乳腺癌。在这里,我们通过 miRNA 微阵列和实时 PCR 分析了 21 例 DCIS 及相应正常组织中的 miRNA 表达谱。miR-10b、miR-125b、miR-132、miR-145、miR-154-3p、miR-382-5p 和 miR-409-3p 在 DCIS 中表达明显下调。CCK-8 检测结果表明,miR-132 的过表达可抑制乳腺癌细胞系的增殖。miR-132 的高表达也可抑制集落形成。我们的研究结果将进一步加深对乳腺癌发展的认识。

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