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GPR37 promotes colorectal cancer against ferroptosis by reprogramming lipid metabolism via p38-SCD1 axis.
Zhou, Jiamin; He, Xigan; Dai, Weixing; Li, Qingguo; Xiang, Zhen; Wang, Yixiu; Zhang, Ti; Xu, Weiqi; Wang, Lu; Mao, Anrong.
Afiliación
  • Zhou J; Department of Hepatic Surgery, Shanghai Cancer Center, Fudan University, Shanghai, 200032, P. R. China.
  • He X; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
  • Dai W; Department of Hepatic Surgery, Shanghai Cancer Center, Fudan University, Shanghai, 200032, P. R. China.
  • Li Q; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
  • Xiang Z; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
  • Wang Y; Department of Colorectal Surgery, Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
  • Zhang T; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
  • Xu W; Department of Colorectal Surgery, Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
  • Wang L; Department of Hepatic Surgery, Shanghai Cancer Center, Fudan University, Shanghai, 200032, P. R. China.
  • Mao A; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Apoptosis ; 2024 Sep 21.
Article en En | MEDLINE | ID: mdl-39306652
ABSTRACT
Colorectal cancer (CRC) is a prevalent malignant tumor worldwide, leading to significant morbidity and disease burden. Diagnostic indicators and treatment objectives for CRC are urgently needed. This study demonstrates that GPR37, a GPCR receptor, is highly expressed in CRC. Depletion of GPR37 significantly reduced CRC tumor cell growth both in vitro and in vivo. Further tests showed that GPR37 protects cancer cells from ferroptosis by upregulating SCD1 expression, thereby modulating lipid metabolism, suppressing the level of reactive oxygen species, and mitigating ferroptosis. Mechanistic studies have shown that GPR37 modulates lipid metabolism in tumor cells by promoting SCD1 transcription via the MAPK-p38 signaling pathway. Our results reveal the pro-carcinogenic effect of GPR37 in primary CRC and suggest that targeting GPR37 could be a potential therapeutic target for CRC.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Apoptosis Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Apoptosis Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos