3 results match your criteria: "PLA Navy No. 971 Hospital[Affiliation]"

Ginsenoside Rh1 regulates the immune microenvironment of hepatocellular carcinoma via the glucocorticoid receptor.

J Integr Med

November 2024

Department of Traditional Chinese Medicine, PLA Navy No. 971 Hospital, Qingdao 266071, Shandong Province, China. Electronic address:

Article Synopsis
  • Ginsenoside Rh1 (G-Rh1) has potential therapeutic effects on hepatocellular carcinoma (HCC), although its impact was previously unclear, as it has shown effectiveness against other cancers like breast and colon cancer.
  • The study used various methods, including bioinformatics and in vitro & in vivo experiments, to examine G-Rh1's effects on HCC cells and the immune environment of tumors.
  • Results indicated that G-Rh1 did not significantly impact HCC cell growth but improved the immune response by enhancing the infiltration of key immune cells and increasing MHC-I expression, suggesting its role in fighting cancer by modifying the tumor microenvironment.
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Background: The mechanism of recurrence and metastasis of hepatocellular carcinoma (HCC) is complex and challenging. Methyl-CpG binding domain protein 3 (MBD3) is a key epigenetic regulator involved in the progression and metastasis of several cancers, but its role in HCC remains unknown.

Methods: MBD3 expression in HCC was detected by immunohistochemistry and its association with clinicopathological features and patient's survival was analysed.

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Background: pH-sensitive peptides are a relatively new strategy for conquering the poor endosomal release of cationic polymer-mediated transfection. Modification of antimicrobial peptides by exchanging positively-charged residues with negatively-charged glutamic acid residues (Glu) greatly improves its lytic activity at the endosomal pH, which could improve cationic polymer-mediated transfection.

Methods: In the present study, we investigated the effect of the number of Glu substituted for positively-charged residues on the endosomal escape activity of AR-23 and the ability of mutated AR-23 with respect to enhancing cationic polymer-mediated transfection.

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