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Monocyte-cancer cell fusion is mediated by phosphatidylserine-CD36 receptor interaction and induced by ionizing radiation.
PLoS One
January 2025
Division of Cell- and Neurobiology, Department of Biomedical and Clinical Sciences, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Emerging evidence suggests that fusion of cancer cells with leucocytes, such as macrophages, plays a significant role in cancer metastasis and results in tumor hybrid cells that acquire resistance to chemo- and radiation therapy. However, the precise mechanisms behind the leukocyte-cancer cell fusion remain unclear. The present in vitro study explores the presence of fusion between the monocyte cell line (THP-1) and the breast cancer cell line (MCF-7) in relation to the expression of CD36 and phosphatidylserine with and without treatment of these cells with ionizing radiation.
View Article and Find Full Text PDFCD36: a promising therapeutic target in hematologic tumors.
Leuk Lymphoma
December 2024
Department of Hematology, Lanzhou University Second Hospital, Lanzhou, China.
Cluster of differentiation 36 (CD36) is a multiligand receptor with important roles in lipid metabolism, angiogenesis and innate immunity, and its diverse effects may depend on the binding of specific ligands in different contexts. CD36 is expressed not only on immune cells in the tumor microenvironment (TME) but also on some hematopoietic cells. CD36 is associated with the growth, metastasis and drug resistance in some hematologic tumors, such as leukemia, lymphoma and myelodysplastic syndrome.
View Article and Find Full Text PDFProtein-energy restriction-induced lipid metabolism disruption causes stable-to-progressive disease shift in Mycobacterium avium-infected female mice.
EBioMedicine
July 2024
Department of Microbiology, Institute for Immunology and Immunological Disease, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, 03722, South Korea. Electronic address:
Article Synopsis
- The study investigates the effects of low body mass index (BMI) on the progression of Mycobacterium avium complex pulmonary disease (MAC-PD) using a specialized mouse model.
- It found that a low protein diet (LPD) worsens MAC-PD progression by disrupting lipid metabolism, leading to increased fatty acid levels and macrophage lipid accumulation during MAC infection.
- The research suggests that improving nutrient intake could help manage MAC-PD, highlighting the importance of host immune cell metabolism and the potential for targeting CD36 pathways as a treatment strategy.
Unveiling the hidden role of the interaction between CD36 and FcγRIIb: implications for autoimmune disorders.
Cell Mol Biol Lett
May 2024
State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Department of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University, Harbin, China.
Article Synopsis
- The study focuses on the role of the scavenger receptor CD36 in B cells, which has not been thoroughly investigated compared to its effects in other immune cells like macrophages and T cells.
- Researchers used Cd36MB1 mice, which lack CD36 specifically in B cells, to study the impact of CD36 on autoimmune responses and performed mass spectrometry to identify proteins interacting with CD36.
- Findings showed that CD36 is crucial for the regulation of autoimmunity in B cells, as its absence led to fewer germinal center B cells and anti-DNA antibodies, and uncovered a new interaction between CD36 and FcγRIIb that could be targeted for autoimmune treatments.
Mitochondria targeted drug delivery system overcoming drug resistance in intrahepatic cholangiocarcinoma by reprogramming lipid metabolism.
Biomaterials
September 2024
State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200032, China. Electronic address:
The challenge of drug resistance in intrahepatic cholangiocarcinoma (ICC) is intricately linked with lipid metabolism reprogramming. The hepatic lipase (HL) and the membrane receptor CD36 are overexpressed in BGJ398-resistant ICC cells, while they are essential for lipid uptake, further enhancing lipid utilization in ICC. Herein, a metal-organic framework-based drug delivery system (OB@D-pMOF/CaP-AC, DDS), has been developed.
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