PDF(Pubmed)
Abstract：
Enforcing a well-differentiated state on cells requires tumor suppressor p53 activation as a key player in apoptosis induction and well differentiation. In addition, recent investigations showed a significant correlation between poorly differentiated status and higher expression of NANOG. Inducing the expression of NANOG and decreasing p53 level switch the status of liver cancer cells from well differentiated to poorly status. In this review, we highlighted p53 and NANOG cross-talk in hepatocellular carcinoma (HCC) which is regulated through mitophagy and makes it a novel molecular target to attenuate cancerous phenotype in the management of this tumor.
摘要：
在细胞上实施良好分化状态需要肿瘤抑制因子p53激活作为凋亡诱导和良好分化的关键角色。此外,最近的研究表明,低分化状态与NANOG的高表达之间存在显著的相关性.诱导NANOG的表达和降低p53水平将肝癌细胞的状态从高分化状态转换为低分化状态。在这次审查中,我们强调了p53和NANOG在肝细胞癌（HCC）中的串扰，它是通过线粒体自噬调节的，并使其成为一种新的分子靶标，以减轻这种肿瘤的治疗中的癌表型。
