Suppr超能文献

微小RNA-769-5p与前列腺癌复发相关,并调节癌细胞的增殖和凋亡。

miR-769-5p is associated with prostate cancer recurrence and modulates proliferation and apoptosis of cancer cells.

作者信息

Lee Daniel

机构信息

Medical Oncology Service and The Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Exp Ther Med. 2021 Apr;21(4):335. doi: 10.3892/etm.2021.9766. Epub 2021 Feb 8.

Abstract

MicroRNAs (miRs) are relevant in biological processes, including human prostate cancer. In the present study, the role of miR-769-5p and its targets in prostate cancer were explored. Publicly available data on expression of genes, miRs and disease-free survival of patients with prostate cancer were analyzed along with RNAseq of transfected cell lines. miR-769-5p expression was inversely associated with patient survival and assays indicated that its inhibition reduced the proliferation and increased apoptosis of prostate cancer cells. miR-769-5p was revealed to target Rho GTPase activating protein 10 (ARHGAP10) and increased expression of ARHGAP10 in tumors was determined to be associated with a favorable prognosis regarding disease-free survival. Of note, ARHGAP10 is a purported tumor suppressor in ovarian cancer, where it inhibits cell division cycle 42 (CDC42) activity and increases apoptosis. Similar effects were observed in prostate cancer cells, where miR-769-5p inhibition increased ARHGAP10 and led to reduced CDC42 activity. Furthermore, miR-769-5p inhibition increased apoptosis, which was partly reversed by additional knockdown of ARHGAP10. These results suggested that miR-769-5p is an oncogene targeting ARHGAP10, which in turn is a candidate tumor suppressor in prostate cancer.

摘要

微小RNA(miR)与包括人类前列腺癌在内的生物过程相关。在本研究中,探讨了miR-769-5p及其靶点在前列腺癌中的作用。分析了前列腺癌患者基因、miR表达及无病生存的公开可用数据,并对转染细胞系进行了RNA测序。miR-769-5p的表达与患者生存呈负相关,实验表明其抑制作用可降低前列腺癌细胞的增殖并增加其凋亡。研究发现miR-769-5p靶向Rho GTP酶激活蛋白10(ARHGAP10),肿瘤中ARHGAP10表达增加被确定与无病生存的良好预后相关。值得注意的是,ARHGAP10在卵巢癌中被认为是一种肿瘤抑制因子,它可抑制细胞分裂周期42(CDC42)的活性并增加凋亡。在前列腺癌细胞中也观察到了类似的效应,miR-769-5p抑制可增加ARHGAP10并导致CDC42活性降低。此外,miR-769-5p抑制可增加凋亡,而ARHGAP10的进一步敲低可部分逆转这种凋亡。这些结果表明,miR-769-5p是一种靶向ARHGAP10的癌基因,而ARHGAP10反过来又是前列腺癌中的候选肿瘤抑制因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a682/7903391/39efdc2f059c/etm-21-04-09766-g00.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验