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2
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本文引用的文献

1
Effect of circulating tumor cells combined with negative enrichment and CD45-FISH identification in diagnosis, therapy monitoring and prognosis of primary lung cancer.循环肿瘤细胞联合阴性富集及CD45荧光原位杂交鉴定在原发性肺癌诊断、治疗监测及预后中的作用
Med Oncol. 2014 Dec;31(12):240. doi: 10.1007/s12032-014-0240-0. Epub 2014 Nov 1.
2
Knockdown of Merm1/Wbscr22 attenuates sensitivity of H460 non-small cell lung cancer cells to SN-38 and 5-FU without alteration to p53 expression levels.敲低Merm1/Wbscr22可减弱H460非小细胞肺癌细胞对SN-38和5-氟尿嘧啶的敏感性,而不会改变p53的表达水平。
Mol Med Rep. 2015 Jan;11(1):295-302. doi: 10.3892/mmr.2014.2764. Epub 2014 Oct 24.
3
Activation of caspases and inhibition of ribosome biogenesis mediate antitumor activity of Chijongdan in A549 non-small lung cancer cells.细胞凋亡蛋白酶的激活和核糖体生物发生的抑制介导赤芝丹在 A549 非小细胞肺癌细胞中的抗肿瘤活性。
BMC Complement Altern Med. 2014 Oct 27;14:420. doi: 10.1186/1472-6882-14-420.
4
[Inhibitory effect of endostar on lymphangiogenesis in non-small cell lung cancer and its effect on circulating tumor cells].恩度对非小细胞肺癌淋巴管生成的抑制作用及其对循环肿瘤细胞的影响
Zhongguo Fei Ai Za Zhi. 2014 Oct 20;17(10):722-9. doi: 10.3779/j.issn.1009-3419.2014.10.03.
5
XBP1 induces snail expression to promote epithelial- to-mesenchymal transition and invasion of breast cancer cells.XBP1诱导蜗牛蛋白表达,以促进乳腺癌细胞的上皮-间质转化和侵袭。
Cell Signal. 2015 Jan;27(1):82-9. doi: 10.1016/j.cellsig.2014.09.018. Epub 2014 Oct 2.
6
[Effect of silencing Bmi-1 expression in reversing cisplatin resistance in lung cancer cells and its mechanism].[沉默Bmi-1表达对逆转肺癌细胞顺铂耐药性的影响及其机制]
Nan Fang Yi Ke Da Xue Xue Bao. 2014 Jun;34(7):1000-4.
7
Bmi-1 regulates epithelial-to-mesenchymal transition to promote migration and invasion of breast cancer cells.Bmi-1调节上皮-间质转化以促进乳腺癌细胞的迁移和侵袭。
Int J Clin Exp Pathol. 2014 May 15;7(6):3057-64. eCollection 2014.
8
[6]-shogaol inhibits growth and induces apoptosis of non-small cell lung cancer cells by directly regulating Akt1/2.[6]-姜烯酚通过直接调控 Akt1/2 抑制非小细胞肺癌细胞的生长并诱导其凋亡。
Carcinogenesis. 2014 Mar;35(3):683-91. doi: 10.1093/carcin/bgt365. Epub 2013 Nov 26.
9
Global Decrease of Histone H3K27 Acetylation in ZEB1-Induced Epithelial to Mesenchymal Transition in Lung Cancer Cells.ZEB1 诱导的肺癌细胞上皮间质转化中组蛋白 H3K27 乙酰化的全球减少。
Cancers (Basel). 2013 Apr 3;5(2):334-56. doi: 10.3390/cancers5020334.
10
Rubus idaeus L. reverses epithelial-to-mesenchymal transition and suppresses cell invasion and protease activities by targeting ERK1/2 and FAK pathways in human lung cancer cells.悬钩子可通过靶向人肺癌细胞中的ERK1/2和FAK通路逆转上皮-间质转化并抑制细胞侵袭和蛋白酶活性。
Food Chem Toxicol. 2013 Dec;62:908-18. doi: 10.1016/j.fct.2013.10.021. Epub 2013 Oct 24.

RNA干扰介导的富含脯氨酸基因的沉默导致人肺癌细胞生长减缓。

RNAi-mediated silencing of praline-rich gene causes growth reduction in human lung cancer cells.

作者信息

Zhao Qingbo

机构信息

Department of Emergency, 324 Hospital of The Chinese People's Liberation Army Chongqing 400020, China.

出版信息

Int J Clin Exp Pathol. 2015 Feb 1;8(2):1760-7. eCollection 2015.

PMID:25973065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4396257/
Abstract

Lung cancer ranks among one of the most frequent causes of cancer death in the world. Here, we investigated PRR11, one novel gene, with no functional annotation, was found to be over-expressed in lung cancer patients suggesting its potential implication in tumorigenesis. Furthermore, high PRR11 levels predict shorter survival of lung cancer patients. In this study, we investigated the therapeutic potential of PRR11 in lung cancer using the technique of RNA silencing via small interfering RNA (siRNA). Synthetic siRNA duplexes against PRR11 were introduced into 3 lung cancer cell lines, which subsequently resulted in a significant depletion in PRR11 expression in the cells. We found that the targeted depletion of PRR11 caused a dramatic cell cycle arrest followed by massive apoptotic cell death, and eventually resulted in a significant decrease in growth and viability of all 2 lung cancer cell lines. In summary, our study strongly suggests that PRR11 may serve as a potential therapeutic target in human lung cancer.

摘要

肺癌是全球癌症死亡的常见原因之一。在此,我们研究了PRR11,这是一个无功能注释的新基因,发现在肺癌患者中过度表达,提示其在肿瘤发生中可能发挥作用。此外,PRR11高水平预示肺癌患者生存期较短。在本研究中,我们通过小干扰RNA(siRNA)技术利用RNA沉默研究了PRR11在肺癌中的治疗潜力。针对PRR11的合成siRNA双链体被导入3种肺癌细胞系,随后导致细胞中PRR11表达显著降低。我们发现靶向敲低PRR11导致细胞周期显著停滞,随后大量细胞凋亡死亡,并最终导致所有2种肺癌细胞系的生长和活力显著下降。总之,我们的研究强烈提示PRR11可能是人类肺癌的潜在治疗靶点。