HIF1α/CCL7/KIAA1199 axis mediates hypoxia-induced gastric cancer aggravation and glycolysis alteration.

IF 2 4区 医学 Q3 NUTRITION & DIETETICS Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-05-01 DOI:10.3164/jcbn.22-48
Chen Mi, Yan Zhao, Li Ren, Dan Zhang
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Abstract

Gastric cancer is a common digestion tumor with high malignant severity and prevalence. Emerging studies reported C-C motif chemokine ligand 7 (CCL7) as a regulator of various tumor diseases. Our research explored the function and underlying mechanism of CCL7 during gastric cancer development. RT-qPCR, Western blot and other datasets were employed to evaluate CCL7 expression in tissues and cells. Kaplan-Meier and Cox regression analyses were recruited to evaluate the correlations between CCL7 expression and patients' survival or clinical features. A loss-of-function assay was performed to evaluate the function of CCL7 in gastric cancer. 1% O2 was utilized to mimic hypoxic condition. KIAA1199 and HIF1α were included in the regulatory mechanism. The results showed that CCL7 was up-regulated and its high expression was correlated with poor survival of gastric cancer patients. Depressing CCL7 attenuated proliferation, migration, invasion, and induced apoptosis of gastric cancer cells. Meanwhile, CCL7 inhibition weakened hypoxia-induced gastric cancer aggravation. Besides, KIAA1199 and HIF1α were involved in the mechanism of CCL7-mediated gastric cancer aggravation under hypoxia. Our research identified CCL7 as a novel tumor-activator in gastric cancer pathogenesis and hypoxia-induced tumor aggravation was regulated by HIF1α/CCL7/KIAA1199 axis. The evidence may provide a novel target for gastric cancer treatment.

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HIF1α/CCL7/KIAA1199轴介导缺氧诱导的胃癌加重和糖酵解改变。
胃癌是一种常见的消化系统肿瘤,恶性程度高,发病率高。新研究报道了C-C基序趋化因子配体7 (CCL7)作为多种肿瘤疾病的调节因子。我们的研究探讨了CCL7在胃癌发生发展中的作用及其机制。采用RT-qPCR、Western blot等数据检测CCL7在组织和细胞中的表达。采用Kaplan-Meier和Cox回归分析评估CCL7表达与患者生存或临床特征的相关性。通过功能丧失测定来评估CCL7在胃癌中的功能。1% O2模拟缺氧状态。KIAA1199和HIF1α参与了调控机制。结果显示,CCL7上调,其高表达与胃癌患者生存不良相关。抑制CCL7可减弱胃癌细胞的增殖、迁移、侵袭并诱导凋亡。同时,CCL7抑制可减弱缺氧诱导的胃癌加重。此外,KIAA1199和HIF1α参与了ccl7介导的缺氧条件下胃癌恶化的机制。我们的研究发现CCL7在胃癌发病过程中是一种新的肿瘤激活因子,缺氧诱导的肿瘤加重受HIF1α/CCL7/KIAA1199轴的调控。这一证据可能为胃癌治疗提供新的靶点。
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来源期刊
CiteScore
4.30
自引率
8.30%
发文量
57
审稿时长
6-12 weeks
期刊介绍: Journal of Clinical Biochemistry and Nutrition (JCBN) is an international, interdisciplinary publication encompassing chemical, biochemical, physiological, pathological, toxicological and medical approaches to research on lipid peroxidation, free radicals, oxidative stress and nutrition. The Journal welcomes original contributions dealing with all aspects of clinical biochemistry and clinical nutrition including both in vitro and in vivo studies.
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