Researchers at Toho University have uncovered a previously unrecognized mechanism controlling how dying cells release the inflammatory cytokine IL-33, a key driver of allergy, asthma, tissue inflammation, and cancer progression. The findings reveal that cells do not release IL-33 uniformly; instead, individual cells exhibit striking differences in release timing controlled by the membrane rupture protein NINJ1.

While many American adults are trying to reduce cholesterol levels, certain cancerous tumors have a relentless appetite for the metabolite. Some tumor cells use as much cholesterol as they can access to accelerate their growth beyond the capabilities of normal cells. 

Marine animals have spent hundreds of millions of years evolving short protein fragments that fight microbes, calm inflammation, and tame tumors. A new review in the Chinese Journal of Natural Medicines maps how researchers are finally catching up: extracting these peptides at scale, decoding their structures with high-resolution mass spectrometry, and using AI to predict which ones might become drugs. The global market for marine peptides already tops USD 310 million, and the authors argue the next wave of therapies for hypertension, diabetes, cancer, and drug-resistant infections may come from the bottom of the food chain.

A new study reveals that many oral cancers are no longer driven by traditional risk factors like smoking or Human papillomavirus infection. Instead, they arise from internal DNA damage and possible microbial influences. By analyzing tumor mutation patterns, researchers identified a distinct subtype of oral squamous cell carcinoma marked by immune evasion and antibacterial responses. These findings reshape our understanding of oral cancer and open the door to more precise, targeted treatments in the future.

Kyoto, Japan -- Like schools of fish and flocks of birds, our cells too can migrate collectively in coordination with their neighbors. This harmonious movement of cells occurs during embryonic development, wound healing, and cancer metastasis. However, since individual cells can only sense limited local information, how they are able to coordinate as a larger collective has remained poorly understood.

Previous studies have demonstrated that this collective migration involves adhesion between cells and waves of ERK signaling activation, named for the ERK proteins involved, and may also be influenced by ZO-1, a scaffolding protein best known for its role in cell-cell adhesion. Building on this knowledge, a team of researchers at Kyoto University was motivated to uncover the elusive mechanism behind collective cell movement.

Using live-cell imaging of Madin-Darby canine kidney cells -- model mammal cells often used in biomedical studies -- the researchers were able to directly observe the movement of cell collectives. They simultaneously monitored ERK activity using a FRET biosensor and visualized ZO-1 localization using fluorescently tagged ZO-1.