Scientists uncover new way in which cells tolerate anticancer drugs
Peer-Reviewed Publication
Updates every hour. Last Updated: 11-Aug-2025 00:11 ET (11-Aug-2025 04:11 GMT/UTC)
Tokyo, Japan – Researchers from Tokyo Metropolitan University have discovered a new pathway by which cells counteract the action of alovudine, an important antiviral and anticancer drug. The protein flap endonuclease-1 (Fen1) was found to improve cell tolerance by counteracting the toxic accumulation of another protein, 53BP1. A renewed spotlight on the underappreciated role of Fen1 promises not only new cancer treatments, but a way to gauge the efficacy of existing treatments.
Fighting off pathogens is a tour de force that must happen with speed and precision. A team of researchers at CeMM and MedUni Vienna led by Christoph Bock and Matthias Farlik has investigated how macrophages—immune cells that are the body’s first responders—master this challenge. Their study, published in Cell Systems (DOI: 10.1016/j.cels.2025.101346), offers a time-resolved analysis of the molecular processes that unfold when these cells encounter various pathogens. They developed a new method that combines gene editing and machine learning, which identified key regulators of macrophage immune responses.
The Japanese rhinoceros beetle Trypoxylus dichotomus is a large insect native to Asia, characterized by the large horn of the male. A research team led by Professor Teruyuki Niimi at the National Institute for Basic Biology is investigating the molecular mechanism of horn development and is developing various molecular techniques essential for this research. To date, the team has successfully decoded the whole genome of the Japanese rhinoceros beetle and established a gene function analysis method using RNA interference.
This time, published in Scientific Reports, the team reported the development of a gene function analysis method using electroporation in Trypoxylus dichotomus larvae.
This review introduces a novel paradigm in cancer biology, focusing on the nuclear phosphoinositide (PIPn)-p53 signalosome and its crucial role in regulating cell motility. Traditionally associated with cytoplasmic and membrane-bound signaling, PIPns are now recognized for orchestrating nuclear events including the stabilization of p53 and activation of nuclear AKT. The review emphasizes the interplay between wild-type or mutant p53 and nuclear PIPn metabolism, opening new directions for therapeutic strategies targeting metastasis.