Newsletters

UNC Researcher Wins Major Grant to Study the Role of Endoplasmic Reticulum in T-Cell Metabolism

[UNC School of Medicine] Dr. Jessica Thaxton at the UNC School of Medicine has been awarded a prestigious $700,000 grant from the Mathers Foundation to support research into the role of the endoplasmic reticulum in T cell metabolism and cancer development.

Immune Checkpoints and Immunoregulation in Metabolic Diseases and Cancers: Pathological Mechanisms and Therapeutic Potential

[Signal Transduction and Targeted Therapy] Growing research demonstrates that immune checkpoint pathways, particularly the PD-1/PD-L1 axis, play dual roles in immune regulation and metabolic modulation by orchestrating inflammatory responses and energy metabolism.

Interleukin-33 and Its Receptor: Multifaceted Roles and Emerging Therapeutic Potential

[Nature Reviews Immunology] Scientists describe the effects of IL-33 in various diseases, including viral infections, cancer, graft-versus-host disease, colitis, autoimmunity, chronic obstructive pulmonary disease, asthma and allergy.

AML1-ETO Hijacks a Distal Enhancer of NAT10 to Reprogram Glutathione Metabolism and Sustain Leukemia Stem Cell Stemness

[Proceedings of The National Academy of Sciences of The United States of America] Genetic ablation or pharmacological inhibition of NAT10 restricted the survival and self-renewal of LSCs in primary t(8;21) acute myeloid leukemia (AML) CD34+ cells, as well as in a retroviral AML1-ETO9a-driven t(8;21) AML mouse model.

Stemness As a Systems-Level State: From Ancestral Plasticity to Systemic Control in Regeneration, Aging, and Cancer

[Annual Review of Genetics] The authors examine early-diverging metazoans to reevaluate the evolutionary logic of stemness. Rather than viewing stem cells as exceptional, we argue that cellular plasticity represents a deeply conserved attribute of early life.

POC1A Promotes the Proliferation, Metastasis, and Stemness of Bladder Cancer by Stabilizing BMI1 via USP7

[Oncogene] Researchers investigated a critical molecular mechanism driving advanced bladder cancer (BLCA) progression. In vitro and in vivo analyses indicate that POC1A knockdown inhibits BLCA cell proliferation, metastasis, and stemness.

Abexinostat Attenuates Temozolomide-Resistant Glioma Stem Cells

[Neuro-Oncology] Researchers demonstrated the anti-proliferative effect of Abexinostat (Abx) on both differentiated cells and glioma stem cells (GSC). Abx reduced both DNA repair machinery and GSC markers by decreasing chromatin accessibility.

NRF2-WNT5A Promotes Stem Cell Persistence and Radioresistance in Esophageal Squamous Cancer

[Cell Death & Disease] Integrating 3D cancer spheroid models with RNA-seq analysis, the authors investigated NRF2 hyperactivation in CSCs and its role as a core mediator of CSC-associated radioresistance and stemness via the canonical WNT/β-catenin pathway.

Stanniocalcin 1 Contributes to Glioma Stem Cells Phenotypic Plasticity through NOTCH1/STAT3/GFPT2 Axis

[Oncogenesis] Investigators revealed that stanniocalcin 1 (STC1) is a key regulator of GSC phenotypic plasticity and aggressiveness through the NOTCH1/STAT3/GFPT2/O-GlcNAcylation pathway.

NKCC1 As a Regulator of Stemness and Redox Balance in Colorectal Cancer

[Oncogenesis] Scientists identified NKCC1 as a marker of normal intestinal stem cells, supported by its crypt-base localization, single-cell transcriptomics, and patient-derived organoids, while analyses of public colorectal cancer single-cell datasets further link NKCC1 expression to cancer stem cell populations.

Glycolytic Enolase 1-Induced H4K12 Lactylation Activates Quiescent Breast Cancer Stem-Like Cells in Triple-Negative Breast Cancer

[Signal Transduction and Targeted Therapy] Researchers developed a dual-reporter system combining NANOG-EGFP and H2B-mCherry pulse-chase labeling to separately identify quiescent or extremely slow-cycling breast cancer stem-like cells and active BCSCs in vitro and in vivo.

The NLRP3 Inflammasome at the Crossroads of Innate Immune Signaling and Cell Death

[Cellular & Molecular Immunology] Substantial crosstalk exists between NLRP3 and other inflammasomes and programmed cell death pathways. The authors summarize recent advances in our understanding of the molecular mechanisms that mediate these interactions, focusing on shared signaling components, organelle dynamics, and posttranslational modifications.
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