Citrulline facilitates the glycolysis, proliferation, and metastasis of lung cancer cells by regulating RAB3C

糖酵解 转移 肺癌 瓜氨酸 癌症 细胞生长 化学 癌症研究 细胞生物学 生物化学 生物 新陈代谢 内科学 医学 遗传学 精氨酸 氨基酸
作者
Qing‐Jun Meng,Yanguang Li,Zhen Sun,Jun‐Feng Liu
出处
期刊:Environmental Toxicology [Wiley]
卷期号:39 (9): 4372-4384 被引量:2
标识
DOI:10.1002/tox.24326
摘要

Abstract Lung cancer (LC) is one of the major malignant diseases threatening human health. The study aimed to identify the effect of citrulline on the malignant phenotype of LC cells and to further disclose the potential molecular mechanism of citrulline in regulating the development of LC, providing a novel molecular biological basis for the clinical treatment of LC. The effects of citrulline on the viability, proliferation, migration, and invasion of LC cells (A549, H1299) were validated by CCK‐8, colony formation, EdU, and transwell assays. The cell glycolysis was assessed via determining the glucose uptake, lactate production, ATP levels, extracellular acidification rate (ECAR), and oxygen consumption rate (OCR). RNA‐seq and molecular docking were performed to screen for citrulline‐binding target proteins. Western blotting experiments were conducted to examine the expression of related signaling pathway molecules. In addition, the impacts of citrulline on LC growth in vivo were investigated by constructing mouse models. Citrulline augmented the viability of LC cells in a concentration and time‐dependent manner. The proliferation, migration, invasion, glycolysis, and EMT processes of LC cells were substantially enhanced after citrulline treatment. Bioinformatics analysis indicated that citrulline could bind to RAB3C protein. Western blotting results indicated that citrulline activated the IL‐6/STAT3 pathway by binding to RAB3C. In addition, animal experiments disclosed that citrulline promoted tumor growth in mice. Citrulline accelerated the glycolysis and activated the IL6/STAT3 pathway through the RAB3C protein, consequently facilitating the development of LC.
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