中文摘要：

mitochondrial 抄写结束因素(MTERF ) 家庭是一组高度保存的 DNA 有约束力的蛋白质 composedof 四个关键成员， MTERF14。迄今为止，几研究在 mitochondrial genomeand 上调查了 MTERF1 的有约束力的地点 mitochondrial 基因抄写的规定，而是在 mitochondrial 基因 transcriptionregulation 之间的更复杂的连接， mitochondrial 氧化 phosphorylation (OXPHOS ) ，和房间增长仍然糟糕被理解。在这研究，我们构造了在表示上和是进 HeLa 房间的 transfected 调查 MTERF1 的功能的 MTERF1 的击倒的向量。结果证明尽管 MTERF1 是 mitochondrial 基因抄写的一个 positiveregulatory 因素，它没在 MTERF1 的 mitochondrial DNA.Over表示的复制上有重要效果增加的 mitochondrial 氧化 phosphorylation 活动和支持的 ATP 合成， cyclin D1expression ，和房间增长它的击倒的禁止的 ATP 合成，减少的 cyclin D1 表示，并且 slowedthe 房间生长。这些结果建议 MTERF1 可以由在 HeLa 房间调整氧化 phosphorylationactivity 支持房间增长。最终，这些调查结果由提供新奇卓见进位于房间增长下面的潜在的机制在 MTERF 家庭的 physiologicalfunctions 上为进一步、更最后的研究创造一个基础规定。

英文摘要：

The mitochondrial transcription termination factor （MTERF） family is a group of highly conserved DNA-binding proteins composed of four key members, MTERF1-4. To date, several studies have investigated the binding sites of MTERF1 on mitochondrial genome and the regulation of mitoehondrial gene transcription, but the more intricate connection between mitochondrial genes transcription regulation, mitochondrial oxidative phosphorylation （OXPHOS）, and cell proliferation is still poorly understood. In this study, we constructed over- expression and knockdown vectors of MTERF1 that were transfected into HeLa cells to investigate the functions of MTERF1. Results showed that although MTERF1 is a positive regulatory factor of mitochondrial genes transcription, it had no significant effect on the replication of mito chondrial DNA. Over-expression of MTERF1 increased mitochondrial oxidative phosphorylation activity and pro moted ATP synthesis, cyclin D1 expression, and cell prolifer ation, while its knockdown inhibited ATP synthesis, decreased cyclin D1 expression, and slowed the cell growth. These results suggested that MTERF1 may promote cell proliferation by regulating oxidative phosphorylation activity in HeLa cells. Ultimately, these findings create a foundation for further and more conclusive studies on the physiological functions of MTERF family by providing novel insights into the potential mechanisms underlying cell proliferation regulation.