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Zhang, C. Z.

Publications and source records attributed to Zhang, C. Z..

2 recordsLinked to original sources

Mechanistic basis of lineage restriction

Lineage restriction is the biological phenomenon where cells lose developmental potency during differentiation for all except their adopted lineages. Lineage restriction is foundational to multicellularity as it secures the functional identities of the myriad cell types in the body. As yet, the mechanisms of lineage restriction remain enigmatic. By developing Potency-Seq to systematically map transcriptional potency of genes across the genome, we uncovered a link between the restriction of developmental potency of cells and the occlusion of transcriptional potency of their genomes. We further showed that, strikingly, genes can undergo irreversible occlusion of their transcriptional potency simply by chromatinization into the nucleosomal form with unmodified histones. These findings led to a comprehensive mechanistic account of lineage restriction as driven by gene occlusion. Specifically, naive pluripotent stem cells at the onset of development possess the unique capacity to erase occlusion globally to reset full transcriptional potency of the genome, which in turn establishes full developmental potency of the cells. Such deocclusion capacity is abolished when cells progress from naive to primed pluripotency. From this stage onward, lineage-inappropriate genes can undergo nucleosome-mediated occlusion in an irreversible manner when their cognate transcription factors (TFs) and/or placeholder factors (PFs) no longer exist in cells to protect them. Consequently, the transcriptionally potent portion of the genome shrinks progressively and irreversibly during differentiation, thus permanently restricting the developmental potency of differentiating cells. ONE-SENTENCE SUMMARYDevelopmental potency of cells is linked to transcriptional potency of their genomes

developmental biology↗

A GYS2/p53 negative feedback loop restricts tumor growth in HBV-related hepatocellular carcinoma

Hepatocarcinogenesis is attributed to the reprogramming of cellular metabolism as consequence of the alteration in metabolite-related gene regulation. Identifying the mechanism of aberrant metabolism is of great potential to provide novel targets for the treatment of hepatocellular carcinoma (HCC). Here, we demonstrated that glycogen synthase 2 (GYS2) restricted tumor growth in HBV-related HCC via a negative feedback loop with p53. Expression of GYS2 was significantly downregulated in HCC and correlated with decreased glycogen content and unfavorable patient outcomes. GYS2 overexpression suppressed, whereas GYS2 knockdown facilitated cell proliferation in vitro and tumor growth in vivo via modulating p53 expression. GYS2 competitively bound to MDM2 to prevent p53 from MDM2-mediated ubiquitination and degradation. Furthermore, GYS2 enhanced the p300-induced acetylation of p53 at K373/382, which in turn inhibited the transcription of GYS2 in the support of HBx/HDAC1 complex. In summary, our findings suggest that GYS2 serves as a prognostic factor and functions as a tumor suppressor in HCC. The newly identified HBx/GYS2/p53 axis is responsible for the deregulation of glycogen metabolism and represents a promising therapeutic target for the clinical management of HCC.\n\nSynopsisThis study elucidate the role of GYS2 in glycogen metabolism and the progression of HCC. The newly identified HBx/GYS2/p53 axis is responsible for the deregulation of glycogen metabolism and represents a promising therapeutic target for the clinical management of HCC.\n\nO_LIDecrease of GYS2 was significantly correlated with decreased glycogen content and unfavorable patient outcomes in a large cohort containing 768 patients with HCC.\nC_LIO_LIGYS2 overexpression suppressed, whereas GYS2 knockdown facilitated cell proliferation in vitro and tumor growth in vivo via modulating p53 signaling pathway.\nC_LIO_LIGYS2 competitively bound to MDM2 to prevent p53 from MDM2-mediated ubiquitination and degradation.\nC_LIO_LIGYS2 enhanced the p300-induced acetylation of p53 at Lys373/382, which in turn inhibited the transcription of GYS2 in the support of HBx/HDAC1 complex.\nC_LI

pathology↗