Overexpression of hnRNPC2 induces multinucleation by repression of Aurora B in hepatocellular carcinoma cells.
Overexpression of hnRNPC2 induces multinucleation by repression of Aurora B in hepatocellular carcinoma cells.
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hnRNPC2 过表达通过抑制 Aurora B 在肝细胞癌细胞中诱导多核
DOI:
10.3892/ol.2013.1167
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发表时间:
2013-04
期刊:
影响因子:
2.9
通讯作者:
Liu DG
中科院分区:
文献类型:
--
作者:
Sun DQ;Wang Y;Liu DG
Heterogeneous ribonuclear protein C2 (hnRNPC2), an RNA binding protein, is a component of hnRNPC which is upregulated in many tumors. Multinucleation exists in many tumors and is positively correlated with tumor grade. To uncover the correlation between hnRNPC2 and multi-nucleation in hepatocellular carcinoma SMMC-7721 cells, we constructed a pEGFP-hnRNPC2 vector and transfected it into cancer cells. Our results revealed that overexpression of hnRNPC2 induced multinucleation in SMMC-7721 cells. Tracking tests indicated that the induced multinucleated cells were unable to recover to mononuclear cells and finally died as a result of defects in cell division. Furthermore, Aurora B, which was localized at the midbody and plays a role in cytokinesis, was repressed in hnRNPC2-overexpressing cells, whose knockdown by RNA interference also induced multinucleation in SMMC-7721 cells. Quantitative polymerase chain reaction (qPCR) and mRNA-protein co-immunoprecipitation results revealed that Aurora B mRNA did not decrease in hnRNPC2-overexpressing cells, instead it bound more hnRNPC2 and less eIF4E, an mRNA cap binding protein and translational initiation factor. Moreover, hnRNPC2 bound more eIF4E in hnRNPC2-overexpressing cells. These results indicate that hnRNPC2 repressed Aurora B binding with eIF4F, which must bind with Aurora B mRNA in order to initiate its translation. This induced multinucleation in hepatocellular carcinoma cells. In addition, hnRNPC2 accelerated hepatocellular carcinoma cell proliferation. Collectively, these data suggest that hnRNPC2 may be a potential target for hepatocellular carcinoma cell diagnosis and treatment.
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影响因子:
4.3
作者:
Hossain, Mohammad Nazir;Fuji, Michihiko;Ayusawa, Dai
通讯作者:
Ayusawa, Dai
DOI:
10.1073/pnas.1108237108
发表时间:
2011-09-13
影响因子:
11.1
作者:
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通讯作者:
Roberts, Thomas M.
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2.4
作者:
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通讯作者:
Madewell, BR
DOI:
10.1083/jcb.200208092
发表时间:
2003-04-28
期刊:
The Journal of cell biology
影响因子:
--
作者:
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通讯作者:
Peters JM
影响因子:
16.8
作者:
通讯作者:
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