58-kDa微小球蛋白(MSP58)已被報導參與在基因轉錄調控和細胞轉型(transformation)能力。在我們的研究中發現利用干擾RNA降低MSP58的表現會導致細胞分裂不正常進而誘導細胞凋亡(apoptosis)的發生，然而大量表現MSP58會導致類似細胞老化的生長停滯。研究持續大量表現MSP58的人類纖維肉瘤細胞株HT1080中發現細胞生長停滯是由於誘導pRB去磷酸化、CDK的抑制劑p21的表現上升以及端粒酶(telomerase)活性的抑制。進而我們利用干擾RNA在持續表現MSP58的HT1080細胞株中降低p21的表現會阻止MSP58 所誘導的細胞老化。此外，近來我們確認分析一些與MSP58有交互作用的新穎蛋白質如需ATP的染色質重建複體(chromatin remodeling complex)成員與參與端粒酶活性的結合蛋白。總結以上實驗我們提供了MSP58調控基因轉錄和細胞老化的新功能。

The nucleolar 58-kDa microspherule protein (MSP58) has been implicated in functional roles of genes transcriptional regulation and cellular transformation. In our studies, abrogation of the endogenous MSP58 function by small interfering RNA knockdown caused aneuploidy and apoptosis, whereas overexpression of MSP58 gene induced the senescence-like growth arrest in HT1080 cells . Studies in the MSP58 stably expressed clones in HT1080 cells revealed that the growth arrest may in part be accounted for by inducing hypophosphorylation of pRB, up-regulation cyclin-dependent kinase inhibitors p21 and telomerase activity inhibition. In addition, abrogation of the endogenous p21 function by RNA interferences in MSP58 stable clones prevents the induction of senescence. Recently, we identified and characterized some MSP58-interacting proteins that is comprised of a SWI/SNF chromatin remodeling complex sununit and novel telomerase regulators. These results provides a previously uncharacterized biological function of MSP58 in its ability to regulate gene expression and cellular senescence.

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