Ube2c, the ubiquitin-conjugating enzyme E2C, is essential for controlling cell cycle progression. It mediates ubiquitylation chain formation via the K11 linkage and is involved in multiple cellular pathways. Ubiquitination, in which Ube2c plays a part, is crucial for protein stability, subcellular localization, and interactions [1,2].

In lung cancer cells with Kras mutations, Ube2c deletion significantly inhibited tumor formation and extended the lifespan of mice, indicating its role in KrasG12D-induced lung tumorigenesis [1]. In bladder cancer, overexpression of Ube2c increased lymphangiogenesis and promoted lymph node metastasis, while its inhibition attenuated these effects [2]. In endometrial cancer, knockdown of Ube2c led to typical autophagic characteristics, and overexpression promoted tumor growth in xenograft mice [3]. In acute myeloid leukemia, Ube2c knockdown inhibited cell viability, promoted apoptosis, and suppressed tumor formation in a mouse model [4].

In conclusion, Ube2c plays a significant role in cell cycle regulation and is involved in the development and progression of multiple cancers such as lung, bladder, endometrial, and acute myeloid leukemia. Gene knockout and conditional knockout mouse models have been instrumental in revealing these functions, providing potential therapeutic targets for these diseases.