Int J Med Sci
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Colorectal cancer (CRC) is a prevalent malignancy with high morbidity and mortality rates globally. Advances in single-cell sequencing technology have enabled comprehensive analyses of tumor cells at single-cell resolution, providing valuable insights into the molecular mechanisms underlying CRC initiation and progression. In this study, we integrated single-cell sequencing data with the TCGA database to identify key molecular pathways involved in CRC pathogenesis. ⋯ Specifically, we observed aberrant expression of genes involved in sphingolipid biosynthesis and degradation, as well as altered levels of various sphingolipid metabolites in CRC cells. Furthermore, we identified several potential therapeutic targets, including SMPD1, GLTP, B3GALT4, and ST8SIA6, within the sphingolipid metabolism pathway that could be exploited for the development of novel CRC treatments. Overall, our findings provide novel insights into the molecular mechanisms underlying CRC and highlight the importance of targeting phospholipid metabolism, specifically sphingolipid metabolism, as a potential therapeutic strategy for CRC.
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Background: Carotene exists naturally in a complex mixture consisting of alpha (α), beta (β), and gamma (γ)-isoforms. Previous studies investigated the effects of individual carotene isomers on bone rather than their actions in a mixture. Purpose: This study explored the bone-protective properties of palm carotene mixture using both two- and three-dimensional co-culture systems. ⋯ Palm carotene mixture also increased bone volume and osteoblast number in the three-dimensional co-culture system. Conclusion: Palm carotene mixture potentially exhibits beneficial effects on bone by accelerating osteoblast proliferation and suppressing osteoclast maturation. The findings of current study serve as the basis for the further validation through animal experiments and human trials.
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Comparative Study
A comparative analysis of Marburg virus-infected bat and human models from public high-throughput sequencing data.
Marburg virus (MARV) disease (MVD) is an uncommon yet serious viral hemorrhagic fever that impacts humans and non-human primates. In humans, infection by the MARV is marked by rapid onset, high transmissibility, and elevated mortality rates, presenting considerable obstacles to the development of vaccines and treatments. Bats, particularly Rousettus aegyptiacus, are suspected to be natural hosts of MARV. ⋯ Our analysis of differentially expressed genes (DEGs) revealed that these genes are mainly associated with pathways related to the complement system, innate immune response via interferons (IFNs), Wnt/β-catenin signaling, and Hedgehog signaling, which played crucial roles in MARV infection across both models. Furthermore, we also identified several potential compounds that may be useful against MARV infection. These findings offer valuable insights into the mechanisms underlying MARV's pathophysiology and suggest potential strategies for preventing transmission, managing post-infection effects, and developing future vaccines.
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Nucleus accumbens-associated protein 1 (NACC1) regulates various types of biological processes. It is a transcription factor associated with cancer. NACC1 is overexpressed in many human malignancies and can regulate the progression, metastasis, and drug resistance of cancer cells. ⋯ Concurrently, ADAM9 knockdown affected the activity of AML cells by decelerating the growth rate, promoting apoptosis, and blocking cell cycle progression. In addition, the AKT activator SC79 restored the inhibited cell proliferation after NACC1 knockdown and ADAM9 knockdown. In conclusion, our study suggested that the NACC1/ADAM9/PI3K/AKT axis is crucial for sustaining the survival of AML cells, indicating that NACC1 may be a viable target for treating AML.
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Aims: Investigate the role of the apelin/APLNR axis in metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on the progression from metabolic dysfunction-associated simple steatotic liver (MASS) to metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis, with emphasis on liver B cells. Methods: Serum samples from MASLD patients and liver tissues from hepatocellular carcinoma patients were collected to measure apelin and APLNR protein expression. C57BL/6J mouse models of varying MASLD stages were developed using a high-fat diet and CCl4. ⋯ Sequencing and RT-PCR in Raji cells indicate that the apelin/APLNR axis promotes the expression of inflammatory cytokines and extracellular matrix molecules. Conclusion: The apelin/APLNR axis is crucial in MASLD progression. Targeting this axis may offer therapeutic potential to modulate B cell function and mitigate MASLD advancement.