pH-responsive graphene-based nanocarriers: A breakthrough for cancer drug delivery
Peer-Reviewed Publication
Updates every hour. Last Updated: 11-Sep-2025 11:11 ET (11-Sep-2025 15:11 GMT/UTC)
Targeted drug delivery to tumors is crucial for effective and safe treatment of cancer. In a recent breakthrough, researchers from Okayama University have developed a pH-responsive nanomaterial using graphene oxide and polyglycerol for cancer drug delivery. The surface of the developed nanomaterial changes its charge in an acidic tumor environment and enables uptake of drugs by cancer cells while avoiding immune clearance. This innovative approach opens doors to precision-driven and more efficient cancer therapies.
Autophagy is a process in which worn out, toxic or degraded cellular components are swept up and recycled to maintain a healthy living cell. When this process is disrupted or disfunctions, it can lead to diseases such as cancer, neurodegeneration, and heart disease.
All our cells have a self-cleaning system known as autophagy, which degrade unwanted materials. And now researchers from Aarhus University have found an important “switch” regulating this key process. A find that could lead to ways to prevent and eventually treat illnesses such as dementia, ALS and cancer.
A team led by Simon Haas has developed a technology to decode how immune cells talk to each other – revealing how our bodies respond to infections, how miscommunication can trigger autoimmune diseases, and why some people don’t respond to immunotherapies. The study was published in “Nature Methods.”
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Lactic acid (LA) has transitioned from being perceived as a mere glycolytic waste product to a pivotal regulator of tumor–immune crosstalk. Historical milestones—from Scheele’s 1780 isolation from sour milk to Zhao’s 2019 discovery of histone lactylation—reveal an expanding biochemical repertoire that now encompasses pH control, G-protein-coupled receptor (GPR81/132) signaling, post-translational modification via lysine lactylation, and multi-directional metabolic shuttling between cytoplasm, mitochondria, and neighboring cells. Within the tumor microenvironment (TME), high glycolytic flux exports lactate and protons through monocarboxylate transporter 4 (MCT4), acidifying the extracellular milieu to ~6.5–6.8. This acidity degrades extracellular matrix, blunts drug uptake, and, via protonation, neutralizes weak-base chemotherapeutics. Cancer cells exploit the same molecule as fuel: MCT1-mediated uptake drives tricarboxylic acid cycle oxidation, NADPH generation via IDH1, and lactylation of DNA-repair proteins NBS1 and MRE11, enhancing genomic stability and chemoresistance. Concurrently, GPR81-cAMP-PKA-TAZ/TEAD signaling elevates PD-L1 expression, facilitating immune escape.
HOXB13, a B-class homeobox transcription factor, sits at the hub of developmental gene networks yet has emerged as a double-edged sword in human cancer. While indispensable for embryonic patterning and androgen-dependent organogenesis, its expression is frequently hijacked or extinguished by epigenetic, mutational and post-translational events that drive tumour initiation, progression and therapy resistance. Across more than twenty malignancies, the protein acts as either oncogene or tumour suppressor, depending on tissue context, interacting partners and mutational status.