Inhibition of lanosterol synthase linking with MAPK/JNK signaling pathway suppresses endometrial cancer DOI Creative Commons
Liangjian Ma, Wunan Huang, Xiaolei Liang

et al.

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: Feb. 8, 2025

Abstract Endometrial cancer (EC) is a significant health threat to women, with recurrence after treatment posing major challenge. While abnormal cholesterol metabolism has been implicated in EC progression, the underlying mechanisms remain unclear. In this study, we identified lanosterol synthase (LSS) as key mediator associated EC. We found that LSS significantly upregulated tissues. Functional assays revealed promotes cell proliferation and migration, inhibits apoptosis, drives tumor growth vivo. Mechanistically, exerts dual effects by accumulating esters, thereby enhancing growth, activating MAPK/JNK signaling pathway. Importantly, inhibition of specific inhibitor Ro 48-8071 not only reduced suppressed xenograft but also inhibited patient-derived tumor-like clusters (PTCs). These findings establish novel oncogene EC, promoting progression through activation ester accumulation, highlight therapeutic potential targeting treatment.

Language: Английский

Inhibition of lanosterol synthase linking with MAPK/JNK signaling pathway suppresses endometrial cancer DOI Creative Commons
Liangjian Ma, Wunan Huang, Xiaolei Liang

et al.

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: Feb. 8, 2025

Abstract Endometrial cancer (EC) is a significant health threat to women, with recurrence after treatment posing major challenge. While abnormal cholesterol metabolism has been implicated in EC progression, the underlying mechanisms remain unclear. In this study, we identified lanosterol synthase (LSS) as key mediator associated EC. We found that LSS significantly upregulated tissues. Functional assays revealed promotes cell proliferation and migration, inhibits apoptosis, drives tumor growth vivo. Mechanistically, exerts dual effects by accumulating esters, thereby enhancing growth, activating MAPK/JNK signaling pathway. Importantly, inhibition of specific inhibitor Ro 48-8071 not only reduced suppressed xenograft but also inhibited patient-derived tumor-like clusters (PTCs). These findings establish novel oncogene EC, promoting progression through activation ester accumulation, highlight therapeutic potential targeting treatment.

Language: Английский

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