Authors
Luhui Zhong, Min Sun, Di Wu, Yulan Zeng, Min Zhou, Rui Gong, Feifei Gu, Kai Zhang, Xiaoyan Hu, Yue Hu
Published in
International journal of oncology. Volume 69. Issue 3. Epub Jul 17, 2026.
Abstract
Colorectal cancer (CRC) cells reprogram multiple metabolic pathways, including anaerobic glycolysis, lipogenesis and amino acid metabolism, to support their rapid cell division. However, the key regulators driving these metabolic alterations in CRC remain unknown. In the present study, immunohistochemistry staining of a tissue microarray demonstrated that yes‑associated protein 1 (YAP1) was markedly upregulated in CRC tissues and strongly associated with worse patient survival. Knocking down YAP1 inhibited the proliferation and cholesterol accumulation of CRC cells both in vitro cell growth assays and in vivo xenograft model. Mechanistically, western blotting, co‑immunoprecipitation and immunofluorescence assays showed that YAP1 not only transcriptionally upregulated sterol regulatory element binding protein 2 (SREBP2) expression but also physically interacted with it to facilitate its nuclear translocation. This coordinated regulation drove the expression of genes governing de novo cholesterol synthesis and exogenous cholesterol influx. Functional experiments revealed that the SREBP2‑dependent cholesterol metabolic pathway was essential for YAP1‑driven tumorigenesis and proliferation in CRC. These findings uncovered a YAP1‑SREBP2 axis involved in CRC metabolic reprogramming and suggested that targeting this interaction may represent a promising metabolic intervention strategy for CRC management.
PMID:
42464642
Bibliographic data and abstract were imported from PubMed on 17 Jul 2026.
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