Nucleolar TRF2 attenuated nucleolus stress-induced HCC cell-cycle arrest by altering rRNA synthesis.
Nucleolar TRF2 attenuated nucleolus stress-induced HCC cell-cycle arrest by altering rRNA synthesis.
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DOI:
10.1038/s41419-018-0572-3
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发表时间:
2018-05-01
影响因子:
9
通讯作者:
Tong T
中科院分区:
文献类型:
--
作者:
Yuan F;Xu C;Li G;Tong T
The nucleolus is an important organelle that is responsible for the biogenesis of ribosome RNA (rRNA) and ribosomal subunits assembly. It is also deemed to be the center of metabolic control, considering the critical role of ribosomes in protein translation. Perturbations of rRNA synthesis are closely related to cell proliferation and tumor progression. Telomeric repeat-binding factor 2 (TRF2) is a member of shelterin complex that is responsible for telomere DNA protection. Interestingly, it was recently reported to localize in the nucleolus of human cells in a cell-cycle-dependent manner, while the underlying mechanism and its role on the nucleolus remained unclear. In this study, we found that nucleolar and coiled-body phosphoprotein 1 (NOLC1), a nucleolar protein that is responsible for the nucleolus construction and rRNA synthesis, interacted with TRF2 and mediated the shuttle of TRF2 between the nucleolus and nucleus. Abating the expression of NOLC1 decreased the nucleolar-resident TRF2. Besides, the nucleolar TRF2 could bind rDNA and promoted rRNA transcription. Furthermore, in hepatocellular carcinoma (HCC) cell lines HepG2 and SMMC7721, TRF2 overexpression participated in the nucleolus stress-induced rRNA inhibition and cell-cycle arrest.
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影响因子:
3.3
作者:
Casafont, I.;Navascues, J.;Berciano, M. T.
通讯作者:
Berciano, M. T.
影响因子:
44.1
作者:
Ren R;Deng L;Xue Y;Suzuki K;Zhang W;Yu Y;Wu J;Sun L;Gong X;Luan H;Yang F;Ju Z;Ren X;Wang S;Tang H;Geng L;Zhang W;Li J;Qiao J;Xu T;Qu J;Liu GH
通讯作者:
Liu GH
影响因子:
14.9
作者:
Figueiredo LM;Rocha EP;Mancio-Silva L;Prevost C;Hernandez-Verdun D;Scherf A
通讯作者:
Scherf A
影响因子:
4.8
作者:
Christensen, MO;Barthelmes, HU;Mielke, C
通讯作者:
Mielke, C
影响因子:
3.5
作者:
Hung, Sandy S.;Lesmana, Analia;Sanij, Elaine
通讯作者:
Sanij, Elaine