共查询到20条相似文献,搜索用时 62 毫秒
1.
Gong‐Hong Wei Gwenael Badis Michael F Berger Teemu Kivioja Kimmo Palin Martin Enge Martin Bonke Arttu Jolma Markku Varjosalo Andrew R Gehrke Jian Yan Shaheynoor Talukder Mikko Turunen Mikko Taipale Hendrik G Stunnenberg Esko Ukkonen Timothy R Hughes Martha L Bulyk Jussi Taipale 《The EMBO journal》2010,29(13):2147-2160
2.
3.
BEL1‐LIKE HOMEODOMAIN 11 regulates chloroplast development and chlorophyll synthesis in tomato fruit
下载免费PDF全文
![点击此处可从《The Plant journal : for cell and molecular biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Lanhuan Meng Zhongqi Fan Qiang Zhang Cuicui Wang Ying Gao Yikang Deng Benzhong Zhu Hongliang Zhu Jianye Chen Wei Shan Xueren Yin Silin Zhong Donald Grierson Cai‐Zhong Jiang Yunbo Luo Da‐Qi Fu 《The Plant journal : for cell and molecular biology》2018,94(6):1126-1140
4.
5.
6.
7.
8.
9.
Yili Hu Francesco Mauri Jonathan Krell Romain Lara Filipa G Pinho Thameenah Choudhury Adam E Frampton Loredana Pellegrino Dmitry Pshezhetskiy Yulan Wang Jonathan Waxman Michael J Seckl Justin Stebbing 《EMBO reports》2016,17(4):570-584
Here, we show that miR‐515‐5p inhibits cancer cell migration and metastasis. RNA‐seq analyses of both oestrogen receptor receptor‐positive and receptor‐negative breast cancer cells overexpressing miR‐515‐5p reveal down‐regulation of NRAS, FZD4, CDC42BPA, PIK3C2B and MARK4 mRNAs. We demonstrate that miR‐515‐5p inhibits MARK4 directly 3′ UTR interaction and that MARK4 knock‐down mimics the effect of miR‐515‐5p on breast and lung cancer cell migration. MARK4 overexpression rescues the inhibitory effects of miR‐515‐5p, suggesting miR‐515‐5p mediates this process through MARK4 down‐regulation. Furthermore, miR‐515‐5p expression is reduced in metastases compared to primary tumours derived from both in vivo xenografts and samples from patients with breast cancer. Conversely, miR‐515‐5p overexpression prevents tumour cell dissemination in a mouse metastatic model. Moreover, high miR‐515‐5p and low MARK4 expression correlate with increased breast and lung cancer patients' survival, respectively. Taken together, these data demonstrate the importance of miR‐515‐5p/MARK4 regulation in cell migration and metastasis across two common cancers. 相似文献
10.
11.
12.
13.
14.
15.
16.
Xue‐ping Luo 《Cell biochemistry and function》2014,32(3):294-298
The pathogenesis of lung cancer is to be further investigated. Recent reports indicate that phospholipase C ε‐1 (PLCE1) is a critical molecule involved in tumour growth. This study aims to investigate the role of PLCE1 in the regulation of apoptosis in lung cancer cells. In this study, the surgically removed non‐small‐cell lung cancer (NSCLC) tissue was collected from 36 patients. Single NSCLC cells were prepared from the tissue, in which immune cells of CD3+, CD11c+, CD19+, CD68+ and CD14+ were eliminated by magnetic cell sorting. The expression of PLCE1 and p53 was assessed by quantitative real‐time polymerase chain reaction and Western blotting. Apoptosis of NSCLC cells was analysed by flow cytometry. The results showed that, in cultured NSCLC cells, high levels of PLCE1 and low levels p53 were detected; the two molecules showed a negative correlation (p < 0.01). The addition of anti‐PLCE1 antibody increased the expression of p53 in NSCLC cells, which increased the frequency of apoptotic NSCLC cells. We conclude that NSCLC cells express high levels of PLCE1, which suppresses the expression of p53 in NSCLC cells. PLCE1 can be a therapeutic target of NSCLC. Copyright © 2013 John Wiley & Sons, Ltd. 相似文献
17.
18.
19.