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ZAR1/2-Regulated Epigenetic Modifications are Essential for Age-Associated Oocyte Quality Maintenance and Zygotic Activation.
Adv Sci (Weinh)
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Department of Obstetrics and Gynecology, Zhejiang Key Laboratory of Precise Protection and Promotion of Fertility, Zhejiang Provincial Clinical Research Center for Reproductive Health and Disease, Assisted Reproduction Unit, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, China.
The developmental competence and epigenetic progression of oocytes gradually become dysregulated with increasing maternal age. However, the mechanisms underlying age-related epigenetic regulation in oocytes remain poorly understood. Zygote arrest proteins 1 and 2 (ZAR1/2) are two maternal factors with partially redundant roles in maintaining oocyte quality, mainly known by regulating mRNA stability.
View Article and Find Full Text PDFSIGLEC11 promotes M2 macrophage polarization through AKT-mTOR signaling and facilitates the progression of gastric cancer.
J Immunother Cancer
January 2025
Department of General Surgery, Shanghai Key Laboratory of Gastric Neoplasms, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Background: Sialic acid-binding immunoglobulin-like lectins (SIGLECs) are widely expressed on immune cell surfaces, play an important role in maintaining immune homeostasis and regulating inflammatory responses, and are increasingly emerging as potential targets for tumor immunotherapy. However, the expression profile and crucial role of SIGLEC11 in gastric cancer (GC) remain unclear. This study aimed to elucidate the prognostic relevance of SIGLEC11 expression and its role in the immune microenvironment in patients with GC.
View Article and Find Full Text PDFInhibition of HDAC6 elicits anticancer effects on head and neck cancer cells through Sp1/SOD3/MKP1 signaling axis to downregulate ERK phosphorylation.
Cell Signal
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Institute of Medical Science, Ajou University School of Medicine, Suwon, Gyeonggi 16499, Republic of Korea; Department of Biomedical Sciences, Ajou University Graduate School of Medicine, Suwon, Gyeonggi 16499, Republic of Korea. Electronic address:
Oxidative stress caused by reactive oxygen species (ROS) and superoxides is linked to various cancer-related biological events. Extracellular superoxide dismutase (SOD3), an antioxidant enzyme that removes superoxides, contributes to redox homeostasis and has the potential to regulate tumorigenesis. Histone deacetylase 6 (HDAC6), a major HDAC isoform responsible for mediating the deacetylation of non-histone protein substrates, also plays a role in cancer progression.
View Article and Find Full Text PDFc-Myc-targeted therapy in breast cancer: A review of fundamentals and pharmacological Insights.
Gene
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Department of Pharmacology, Federal University of Paraná, Curitiba, PR, Brazil.
The oncoprotein c-Myc is expressed in all breast cancer subtypes, but its expression is higher in triple-negative breast cancer (TNBC) compared to estrogen receptor (ER+), progesterone receptor (PR+), or human epidermal growth factor receptor 2 (HER2+) positive tumors. The c-Myc gene is crucial for tumor progression and therapy resistance, impacting cell proliferation, differentiation, senescence, angiogenesis, immune evasion, metabolism, invasion, autophagy, apoptosis, chromosomal instability, and protein biosynthesis. Targeting c-Myc has emerged as a potential therapeutic strategy for TNBC, a highly aggressive and deadly breast cancer form.
View Article and Find Full Text PDFA non-purine inhibitor of xanthine oxidoreductase mitigates adenosine triphosphate degradation under hypoxic conditions in mouse brain.
Brain Res
January 2025
Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo, Japan. Electronic address:
The brain is an organ that consumes a substantial amount of oxygen, and a reduction in oxygen concentration can rapidly lead to significant and irreversible brain injury. The progression of brain injury during hypoxia involves the depletion of intracellular adenosine triphosphate (ATP) due to decreased oxidative phosphorylation in the inner mitochondrial membrane. Allopurinol is a purine analog inhibitor of xanthine oxidoreductase that protects against hypoxic/ischemic brain injury; however, its underlying mechanism of action remains unclear.
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