Hemangioma (HA) is the most common benign tumor and formed by the proliferating endothelial cells of blood vessels. Interleukins (ILs) have been reported to be critical for HA progression. Our present study found that the expression of IL-10 was decreased in HA cells and tissues as compared to their corresponding controls. Treatment with recombinant IL-10 (rIL-10) can suppress the proliferation of HA cells via suppression of proliferating cell nuclear antigen (PCNA), while over expression of PCNA can attenuate rIL-10-inhibited cell proliferation. Further, rIL-10 can decrease the promoter activity and mRNA stability of PCNA in HA cells. Mechanistically, rIL-10 can increase expression of miR-27b-3p to decrease mRNA stability of PCNA, while down regulation of YY1 is involved in rIL-10 suppressed transcription of PCNA. Collectively, IL-10 can suppress the expression of PCNA via miR-27b-3p mediated suppression of mRNA stability and YY1 mediated down regulation of transcription. It suggested that rIL-10 might be a potential therapeutic approach for HA development and progression.
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http://dx.doi.org/10.1016/j.abb.2020.108404 | DOI Listing |
Redox Rep
December 2025
Department of Cardiology, Fujian Medical University Union Hospital, Fuzhou, Fujian, People's Republic of China.
Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.
Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model.
Cell Mol Life Sci
January 2025
Department of Clinical Laboratory, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, China.
Non-small cell lung cancer (NSCLC) has emerged as one of the most prevalent malignancies worldwide. N6-methyladenosine (mA) methylation, a pervasive epigenetic modification in long noncoding RNAs (lncRNAs), plays a crucial role in NSCLC progression. Here, we report that mA modification and the expression of the lncRNA stem cell inhibitory RNA transcript (SCIRT) was significantly upregulated in NSCLC tissues and cells.
View Article and Find Full Text PDFNucleic Acids Res
January 2025
Centre for Bacterial Resistance Biology, Imperial College London, LondonSW7 2AZ, United Kingdom.
The RNA chaperone Hfq plays crucial roles in bacterial gene expression and is a major facilitator of small regulatory RNA (sRNA) action. The toroidal architecture of the Hfq hexamer presents three well-characterized surfaces that allow it to bind sRNAs to stabilize them and engage target transcripts. Hfq-interacting sRNAs are categorized into two classes based on the surfaces they use to bind Hfq.
View Article and Find Full Text PDFFront Immunol
January 2025
Traditional Chinese Medicine Department of Orthopaedic and Traumatic, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Colorectal cancer (CRC) is one of the most prevalent malignant tumors in the world, and its occurrence and development are closely related to the complex immune regulatory mechanisms. As the first barrier of the body's defense, innate immunity plays a key role in tumor immune surveillance and anti-tumor response, in which type I/III interferon (IFN) is an important mediator with significant antiviral and anti-tumor functions. 5-methylcytosine (m5C) modification of RNA is a key epigenetic regulation that promotes the expression of CRC oncogenes and immune-related genes.
View Article and Find Full Text PDFHeliyon
January 2025
The First Affiliated Hospital of Bengbu Medical University, Department of Vascular Surgery, 287 Changhuai Road, Bengbu, 233004, China.
Objective: M6A methylation-regulated macrophages play an important role in the occurrence and development of arteriosclerosis. However, their role in lower extremity arteriosclerosis remains unclear. Therefore, this study aims to explore the key factors that regulate arteriosclerosis methylation in the lower extremities and the mechanism by which they affect arteriosclerosis by influencing macrophage polarization.
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