Publications by authors named "Yuemei Hong"

The impact of dietary nutrients on tumor immunity remains an area of ongoing investigation, particularly regarding the specific role of vitamins and their mechanism. Here, we demonstrate that vitamin B3 (VB3) induces antitumor immunity against liver cancer through biased GPR109A axis in myeloid cell. Nutritional epidemiology studies suggest that higher VB3 intake reduces liver cancer risk.

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Age-related osteoporosis manifests as a complex pathology that disrupts bone homeostasis and elevates fracture risk, yet the mechanisms facilitating age-related shifts in bone marrow macrophages/osteoclasts (BMMs/OCs) lineage are not fully understood. To decipher these mechanisms, we conducted an investigation into the determinants controlling BMMs/OCs differentiation. We performed single-cell multi-omics profiling on bone marrow samples from mice of different ages (1, 6, and 20 months) to gain a holistic understanding of cellular changes across time.

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Objective: The metabolic characteristics of liver cancer drive considerable hurdles to immune cells function and cancer immunotherapy. However, how metabolic reprograming in the tumour microenvironment impairs the antitumour immune response remains unclear.

Design: Human samples and multiple murine models were employed to evaluate the correlation between GPR109A and liver cancer progression.

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Article Synopsis
  • Candidalysin, a toxin produced by Candida albicans, plays a crucial role in how the fungus causes disease, but its specific interactions with human proteins were not well understood until now.
  • Researchers used a high-throughput method to identify potential human protein targets of eight Ece1 peptides, discovering that CCNH, which is involved in DNA damage repair, interacts with candidalysin.
  • Candidalysin was found to increase the formation of double-strand DNA breaks by activating CCNH, disrupting the DNA repair pathway, which highlights how this fungal toxin may help the fungus persist in infections.
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Colorectal cancer (CRC) is a multifactorial heterogeneous disease largely due to both genetic predisposition and environmental factors including the gut microbiota, a dynamic microbial ecosystem inhabiting the gastrointestinal tract. Elucidation of the molecular mechanisms by which the gut microbiota interacts with the host may contribute to the pathogenesis, diagnosis, and promotion of CRC. However, deciphering the influence of genetic variants and interactions with the gut microbial ecosystem is rather challenging.

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