C1QBP Promotes Prostate Cancer Progression and Lipid Accumulation by Negatively Regulating ALDH9A1

被引:0
作者
Liu, Xinyu [1 ]
Li, Jiaxin [1 ]
Du, Runxuan [2 ,3 ]
Qiao, Qiufang [1 ]
Liu, Shuang [1 ]
Bo, Zhihao [2 ]
Chen, Ruibing [4 ]
Dong, Yihan [1 ]
Xiao, Xuesong [2 ]
Pan, Yuejing [1 ]
Jiang, Huamao [5 ]
Wang, Rui [1 ]
Wang, Yong [2 ]
Yue, Dan [1 ]
机构
[1] Tianjin Med Univ, Sch Med Technol, Tianjin, Peoples R China
[2] Tianjin Med Univ, Tianjin Inst Urol, Dept Urol, Hosp 2, Tianjin, Peoples R China
[3] Tianjin Fifth Cent Hosp, Dept Urol, Tianjin, Peoples R China
[4] Tianjin Univ, Fac Med, Sch Pharmaceut Sci & Technol, Tianjin, Peoples R China
[5] Jinzhou Med Univ, Dept Urol, Affiliated Hosp 1, Jinzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
C1QBP; lipid metabolism; prostate cancer; ALDEHYDE DEHYDROGENASE;
D O I
10.1002/mc.23904
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Prostate cancer (PCa) relies heavily on lipid metabolism for energy acquisition, and lipid metabolic reprogramming plays a crucial role in its progression. Here, we utilized publicly available PCa databases and immunohistochemistry to evaluate C1QBP expression in PCa. We found that C1QBP is highly expressed in PCa, potentially due to promoter hypomethylation. Functional assays showed that C1QBP promotes cell proliferation, migration, and lipid accumulation in PCa cells. We identified differentially expressed proteins associated with C1QBP by using liquid chromatography-tandem mass spectrometry. Functional enrichment analysis revealed that C1QBP affects lipid metabolism and negatively regulates the lipid metabolism-related molecule ALDH9A1. Furthermore, ALDH9A1 intervention rescued the tumor suppression and lipid reduction caused by C1QBP knockdown. RNA sequencing (RNA-seq) was performed to explore C1QBP regulatory pathways at the mRNA level, revealing that C1QBP also affects the MAPK and p53 pathways, as well as the expression of lipid metabolism-related molecules. In conclusion, these findings suggest that C1QBP influences PCa progression and lipid deposition by regulating ALDH9A1, while other potential mechanisms may also be involved, indicating that C1QBP is a promising target for PCa treatment.
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页数:16
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