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长链非编码 RNA HOTTIP 介导的 HOXA11 表达促进乳腺癌细胞的生长、迁移并抑制细胞凋亡。

LncRNA HOTTIP-Mediated HOXA11 Expression Promotes Cell Growth, Migration and Inhibits Cell Apoptosis in Breast Cancer.

机构信息

Department of Pathology, Guangdong Medical University, Dongguan 523808, China.

Department of Radiotherapy, State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou 510060, China.

出版信息

Int J Mol Sci. 2018 Feb 6;19(2):472. doi: 10.3390/ijms19020472.

DOI:10.3390/ijms19020472
PMID:29415429
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5855694/
Abstract

As the most common cause of cancer death in women, the pathogenesis of breast cancer still remains unclear. Here, we reported a long non-coding RNA (lncRNA), HOTTIP (HOXA transcript at the distal tip), that may play an important role in the pathogenesis of breast cancer. Using gain-and-loss-of experiments in vitro and in vivo, we observed the marked upregulation of HOTTIP/HOXA11 in the breast cancer cell line, MCF-7, and the downregulation of HOTTIP or HOXA11, which might inhibit cell proliferation and migration but promote cell apoptosis in breast cancer MCF-7 cells. In addition, by further rescue experiments with HOXA11 overexpression, we uncovered a novel potential regulatory mechanism between HOTTIP and one of its physical HOXA clusters, HOXA11. Hence, HOTTIP may mediate, at least partly, HOXA11 expression involved in cell growth, migration, and apoptosis of breast cancer MCF-7 cells.

摘要

作为女性癌症死亡的最常见原因,乳腺癌的发病机制仍不清楚。在这里,我们报道了一个长非编码 RNA(lncRNA),即 HOXA 转录物远端末端(HOTTIP),它可能在乳腺癌的发病机制中发挥重要作用。通过体外和体内的增益和损失实验,我们观察到乳腺癌细胞系 MCF-7 中 HOTTIP/HOXA11 的显著上调,以及 HOTTIP 或 HOXA11 的下调,这可能抑制乳腺癌 MCF-7 细胞的增殖和迁移,但促进细胞凋亡。此外,通过 HOXA11 过表达的进一步挽救实验,我们揭示了 HOTTIP 和其物理 HOXA 簇之一 HOXA11 之间的一个新的潜在调节机制。因此,HOTTIP 可能至少部分介导了涉及乳腺癌 MCF-7 细胞生长、迁移和凋亡的 HOXA11 表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/501a6c27166b/ijms-19-00472-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/73ffe82f6d00/ijms-19-00472-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/1f3285c54bbf/ijms-19-00472-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/e5407b6aad6d/ijms-19-00472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/501a6c27166b/ijms-19-00472-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/73ffe82f6d00/ijms-19-00472-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/1f3285c54bbf/ijms-19-00472-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/e5407b6aad6d/ijms-19-00472-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff0a/5855694/501a6c27166b/ijms-19-00472-g004a.jpg

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