共查询到20条相似文献,搜索用时 15 毫秒
1.
2.
3.
4.
Overexpression of Long Non‐Coding RNA MEG3 Inhibits Proliferation of Hepatocellular Carcinoma Huh7 Cells via Negative Modulation of miRNA‐664 下载免费PDF全文
Jin‐Hua He Ze‐Ping Han Ji‐Ming Liu Jia‐Bin Zhou Mao‐Xian Zou Yu‐Bing Lv Yu‐Guang Li Ming‐Rong Cao 《Journal of cellular biochemistry》2017,118(11):3713-3721
5.
6.
Chang‐Jiang Lei Ji‐Yu Wen Ming‐Yi Li Zhong‐Kao Liu Zhi‐Dong Qiu Man‐Zhou Lin Nian‐Ping Chen Ming Chen 《Journal of cellular biochemistry》2013,114(3):625-631
Glypican‐3 (GPC3), a membrane‐associated heparan sulfate proteoglycan, is frequently upregulated in hepatocellular carcinoma (HCC). Yes‐associated protein (YAP) is also found over‐expressed in HCC and has been identified as a key effector molecule in Hippo pathway, which could control the organ size in animals through the regulation of cell proliferation and apoptosis and plays an important role in the development of malignant tumors. Studies have reported that GPC3 and YAP might collaborate to regulate the development of HCC. To elucidate the role of GPC3 in the development of HCC and its relationship with YAP, siRNA technique was employed to knock down GPC3 in Huh7 HCC cells. Moreover, recombinant human YAP‐1 was used to examine the effects of GPC3 on Huh7 cells. The results of flow cytometric analysis and Annexin‐V‐FLUOS apoptosis assay showed that knockdown of GPC3‐induced apoptosis in Huh7 cells, resulting in inhibition of cell proliferation as examined by EdU incorporation assay, migration, and invasion. GPC3 knockdown also suppressed the expression of YAP in mRNA and protein levels, as examined by fluorescence quantitative PCR and Western blot analysis. Moreover, addition of recombinant human YAP‐1 effectively rescued the cells from apoptosis triggered by GPC3 knockdown. Taken together, our findings suggest that GPC3 regulates HCC cell proliferation with the involvement of Hippo pathway. J. Cell. Biochem. 114: 625–631, 2013. © 2012 Wiley Periodicals, Inc. 相似文献
7.
8.
9.
Jianrui Song Xianling Guo Xuqin Xie Xue Zhao Ding Li Weijie Deng Yujiao Song Feng Shen Mengchao Wu Lixin Wei 《Journal of cellular biochemistry》2011,112(11):3406-3420
Oxygen deficiency and nutrient deprivation widely exists in solid tumors because of the poor blood supply. However, cancer cells can survive this adverse condition and proliferate continuously to develop. To figure out the way to survive, we investigated the role of autophagy in the microenvironment in hepatocellular carcinoma. In order to simulate the tumor microenvironment more veritably, cells were cultured in oxygen‐nutrient‐deprived condition following a hypoxia preconditioning. As a result, cell death under hypoxia plus nutrient deprivation was much less than that under nutrient deprivation only. And the decreased cell death mainly attributed to the decreased apoptosis. GFP‐LC3 and electron microscopy analysis showed that autophagy was significantly activated in the period of hypoxia preconditioning. However, autophagic inhibitor—3‐MA significantly abrogated the apoptosis reduction in hypoxia, which implied the involvement of autophagy in protection of hepatocellular carcinoma cells against apoptosis induced by starvation. Furthermore, Beclin 1 was proved to play an important role in this process. siRNA targeting Beclin 1 was transfected into hepatocellular carcinoma cells. And both data from western blot detecting the expression of LC3‐II and transmission microscopy observing the accumulation of autophagosomes showed that autophagy was inhibited obviously as a result of Beclin 1 knockdown. Besides, the decreased apoptosis of starved cells under hypoxia was reversed. Taken together, these results suggest that autophagy activated by hypoxia mediates the tolerance of hepatocellular carcinoma cells to nutrient deprivation, and this tolerance is dependent on the activity of Beclin 1. J. Cell. Biochem. 112: 3406–3420, 2011. © 2011 Wiley Periodicals, Inc. 相似文献
10.
11.
12.
13.
14.
15.
Runt‐Related Transcription Factor 2 (Runx2) Is Responsible for Galectin‐3 Overexpression in Human Thyroid Carcinoma 下载免费PDF全文
Engin Kaptan Serap Sancar Bas Aylin Sancakli Hatice Gumushan Aktas Bertan Boran Bayrak Refiye Yanardag Sehnaz Bolkent 《Journal of cellular biochemistry》2017,118(11):3911-3919
16.
17.
18.
19.
20.