Tumour-suppressor proteins articles from across Nature Portfolio

The deubiquitinase USP24 stabilizes Beclin1 by decreasing its K48-linked ubiquitination. The interaction between USP24 and Beclin1 represents a key molecular mechanism that promotes autophagy related ferroptosis in HCC.

Akiko Takahashi discusses the seminal 1997 paper by Serrano et al. who found that oncogene activation results in a similar phenotype to replicative senescence, establishing the connection between senescence and cancer.

Ciwinska et al. asked whether natural tissue remodelling can drive mutant cell expansion and identified three protective mechanisms in the healthy mouse mammary gland that constrain the ability of mutant cells to transform and give rise to cancer.

The studies that paved the way for the development of PROTACs (proteolysis-targeting chimeras) as therapeutic strategies, and the HPV vaccine.

Lim et al. show that ASS1, silenced in many cancer types, is a metabolic checkpoint that, following DNA damage, halts cell cycle progression by restricting nucleotide synthesis and p53-related gene transcription.

Kong et al. have now shown that Knudson’s two-hit hypothesis can be circumvented through the actions of the glycolytic metabolite methylglyoxal, which transiently inactivates the tumour-suppressive functions of BRCA2 leading to episodic mutagenesis and cancer genome evolution.