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Wang CL, Tang Y, Li M, et al. Cancer Manag Res. 2021;13:2401–2409. Page 2405, Table 4, the column headed “Positivity Rate (%)” should read “Rate (%)”. Table 6 on page 2406 is incorrect. The correct Table 6 is shown below. Page 2406, right column, second line, the text “the reverse Golgi apparatus” should read “the trans Golgi apparatus”. Page 2406, right column, second line from the bottom, the text “protein kinase RNA-like endoplasmic reticulum Kinase” should read “protein kinase R-like endoplasmic reticulum kinase (PERK)”. Page 2407, right column, third sentence, the text “In addition, MARylation of the hydrolases PARG,33 TARG1,34 MACROD235 and PARP136 shifts their activities toward cell damage repair” should read “In addition, the hydrolases PARG33, TARG134, MACROD235 and MARylation of PARP136 shifts their activities toward cell damage repair”. Read the original article

Colorectal cancer (CRC) is a global health concern. The role of epigenetics in tumors has garnered increasing interest. ADP ribosylation is an epigenetic modification that is associated with a variety of biological functions and diseases, and its association with tumor development and progression has been hypothesized. However, due to the limitations of available techniques and methods, ADP ribosylation of specific sites is difficult to determine. In previous studies, it was shown that arginine-117 of histone 3 (H3R117) in Lovo cells can be modified by mono-ADP-ribosylation. This site was mutated and Lovo cells overexpressing this mutant construct were established. In the present study, the expression of differentially expressed genes (DEGs) between untransfected Lovo cells and H3R117A Lovo cells was analyzed. A total of 58,174 DEGs were identified, of which 2,324 were significantly differentially expressed (q-value 2). Functional annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment was used to analyze the functions and possible roles of the DEGs. The DEGs were enriched in pathways associated with metabolic process, catalytic activity, organelle and chromatin structure, and dynamics. Through this comprehensive and systematic analysis, the role of mono-ADP-ribosylation in CRC was examined, providing a foundation for future studies.

Background:Liver kinase B1 (LKB1)/5’-adenosine monophosphate-activated protein kinase (AMPK) signaling, a metabolic checkpoint, plays a neuro-protective role in the pathogenesis of Alzheimer’s disease (AD). Amyloid-β (Aβ) acts as a classical biomarker of AD. The aim of the present study was to explore whether berberine (BBR) activates LKB1/AMPK signaling and ameliorates Aβ pathology.Methods:The Aβ levels were detected using enzyme-linked immunosorbent assay and immunohistochemistry. The following biomarkers were measured by Western blotting: phosphorylated (p-) LKB1 (Ser334 and Thr189), p-AMPK (AMPKα and AMPKβ1), synaptophysin, post-synaptic density protein 95 and p-cAMP-response element binding protein (p-CREB). The glial fibrillary acidic protein (GFAP) was determined using Western blotting and immunohistochemistry.Results:BBR inhibited Aβ expression in the brain of APP/PS1 mice. There was a strong up-regulation of both p-LKB1 (Ser334 and Thr189) and p-AMPK (AMPKα and AMPKβ1) in the brains of APP/PS1 transgenic mice after BBR-treatment (PConclusion:BBR alleviates Aβ pathogenesis and rescues synapse damage via activating LKB1/AMPK signaling in the brain of APP/PS1 transgenic mice.