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本文引用的文献

1
mir-106a regulates cell proliferation and apoptosis of colon cancer cells through targeting the PTEN/PI3K/AKT signaling pathway.微小RNA-106a通过靶向PTEN/PI3K/AKT信号通路调控结肠癌细胞的增殖和凋亡。
Oncol Lett. 2018 Mar;15(3):3197-3201. doi: 10.3892/ol.2017.7715. Epub 2017 Dec 29.
2
Disentangling -cooperating tumor suppressor gene networks in cancer.解析癌症中协同作用的肿瘤抑制基因网络
Mol Cell Oncol. 2017 May 4;4(4):e1325550. doi: 10.1080/23723556.2017.1325550. eCollection 2017.
3
Overexpression of PTEN suppresses non-small-cell lung carcinoma metastasis through inhibition of integrin αVβ6 signaling.PTEN的过表达通过抑制整合素αVβ6信号传导来抑制非小细胞肺癌转移。
Am J Transl Res. 2017 Jul 15;9(7):3304-3314. eCollection 2017.
4
Tumor-suppressive miR-26a and miR-26b inhibit cell aggressiveness by regulating FUT4 in colorectal cancer.肿瘤抑制性miR-26a和miR-26b通过调节结直肠癌中的FUT4来抑制细胞侵袭性。
Cell Death Dis. 2017 Jun 22;8(6):e2892. doi: 10.1038/cddis.2017.281.
5
Loss of PTEN expression in breast cancer: association with clinicopathological characteristics and prognosis.乳腺癌中PTEN表达缺失:与临床病理特征及预后的关联
Oncotarget. 2017 May 9;8(19):32043-32054. doi: 10.18632/oncotarget.16761.
6
MicroRNA-130b targets PTEN to mediate drug resistance and proliferation of breast cancer cells via the PI3K/Akt signaling pathway.微小 RNA-130b 通过 PI3K/Akt 信号通路靶向 PTEN 介导乳腺癌细胞的耐药性和增殖。
Sci Rep. 2017 Feb 6;7:41942. doi: 10.1038/srep41942.
7
PTEN expression is a prognostic marker for patients with non-small cell lung cancer: a systematic review and meta-analysis of the literature.PTEN表达是非小细胞肺癌患者的预后标志物:一项文献的系统评价和荟萃分析
Oncotarget. 2016 Sep 6;7(36):57832-57840. doi: 10.18632/oncotarget.11068.
8
miR-106a promotes growth and metastasis of non-small cell lung cancer by targeting PTEN.微小RNA-106a通过靶向磷酸酶和张力蛋白同源物促进非小细胞肺癌的生长和转移。
Int J Clin Exp Pathol. 2015 Apr 1;8(4):3827-34. eCollection 2015.
9
MicroRNA in prostate cancer: functional importance and potential as circulating biomarkers.前列腺癌中的微小RNA:功能重要性及作为循环生物标志物的潜力
BMC Cancer. 2014 Dec 10;14:930. doi: 10.1186/1471-2407-14-930.
10
Prostate cancer: review in 2014.前列腺癌:2014年综述
Diagn Interv Imaging. 2014 Jul-Aug;95(7-8):739-42. doi: 10.1016/j.diii.2014.06.005. Epub 2014 Jul 16.

微小RNA-106a通过磷酸酶和张力蛋白同源物(PTEN)促进前列腺癌进展。

miR-106a contributes to prostate carcinoma progression through PTEN.

作者信息

Lu Ji, Mu Xupeng, Yin Qinan, Hu Kebang

机构信息

Department of Urology, The First Hospital, Jilin University, Changchun, Jilin 130021, P.R. China.

Department of Central Laboratory, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.

出版信息

Oncol Lett. 2019 Jan;17(1):1327-1332. doi: 10.3892/ol.2018.9697. Epub 2018 Nov 14.

DOI:10.3892/ol.2018.9697
PMID:30655902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6313013/
Abstract

Prostate carcinoma is a global health problem and is estimated to be diagnosed in 1.1 million men/year, making this malignancy the second most frequently diagnosed cancer in males worldwide. micro RNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. miRNAs contribute to cancer development and progression, and are expressed differently in normal tissues and cancers. In the present study, the biological function of miR-106a in the human prostate carcinoma and the associated regulatory mechanisms were investigated. miR-106a was significantly upregulated in human prostate cancer tissues when compared with normal tissues (P<0.05), and the overexpression of miR-106a was identified to promote PC-3 cell growth. Additionally, miRNA-106a inhibition significantly suppressed PC-3 cell growth. Furthermore, it was observed that the phosphatase and tensin homolog (PTEN) expression level was negatively associated with miR-106a expression level, and miRNA-106a directly targeted PTEN in the PC-3 cells. PTEN overexpression has a similar effect on PC-3 cell growth as loss of miR-106a. Taken together, the results of the present study indicate that upregulated miR-106a regulates PC-3 cell proliferation through PTEN. These results suggest that appropriate manipulation of miR-106a may provide a novel strategy in the future treatment of human prostate cancer.

摘要

前列腺癌是一个全球性的健康问题,据估计每年有110万男性被诊断出患有该病,使其成为全球男性中第二大最常被诊断出的癌症。微小RNA(miRNA)是小的非编码RNA,在转录后水平上负调控基因表达。miRNA有助于癌症的发生和发展,并且在正常组织和癌症中表达不同。在本研究中,对miR-106a在人前列腺癌中的生物学功能及其相关调控机制进行了研究。与正常组织相比,miR-106a在人前列腺癌组织中显著上调(P<0.05),并且已确定miR-106a的过表达促进PC-3细胞生长。此外,抑制miRNA-106a可显著抑制PC-3细胞生长。此外,观察到磷酸酶和张力蛋白同源物(PTEN)的表达水平与miR-106a的表达水平呈负相关,并且miRNA-106a在PC-3细胞中直接靶向PTEN。PTEN过表达对PC-3细胞生长的影响与miR-106a缺失类似。综上所述,本研究结果表明上调的miR-106a通过PTEN调节PC-3细胞增殖。这些结果表明,对miR-106a进行适当调控可能为未来人类前列腺癌的治疗提供一种新策略。