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多组学分析结直肠癌中葡萄糖代谢重编程。

Multi-omics analyses of glucose metabolic reprogramming in colorectal cancer.

机构信息

Guangxi Clinical Research Center for Colorectal Cancer, Guangxi Medical University Cancer Hospital, Nanning, Guangxi Zhuang Autonomous Region, China.

Department of Gastrointestinal Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi Zhuang Autonomous Region, China.

出版信息

Front Immunol. 2023 Jul 5;14:1179699. doi: 10.3389/fimmu.2023.1179699. eCollection 2023.

DOI:10.3389/fimmu.2023.1179699
PMID:37475862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10354426/
Abstract

BACKGROUND

Glucose metabolic reprogramming (GMR) is a cardinal feature of carcinogenesis and metastasis. However, the underlying mechanisms have not been fully elucidated. The aim of this study was to profile the metabolic signature of primary tumor and circulating tumor cells from metastatic colorectal cancer (mCRC) patients using integrated omics analysis.

METHODS

PET-CT imaging, serum metabolomics, genomics and proteomics data of 325 high 18F-fluorinated deoxyglucose (FDGhigh) mCRC patients were analyzed. The para-tumor, primary tumor and liver metastatic tissues of mCRC patients were used for proteomics analysis.

RESULTS

The glucose uptake in tumor tissues as per the PET/CT images was correlated to serum levels of glutamic-pyruvic transaminase (ALT), total bilirubin (TBIL), creatinine (CRE). Proteomics analysis indicated that several differentially expressed proteins were enriched in both GMR and epithelial-mesenchymal transition (EMT)-related pathways. Using a tissue-optimized proteomic workflow, we identified novel proteomic markers (e.g. CCND1, EPCAM, RPS6), a novel PCK1-CDK6-INSR protein axis, and a potential role for FOLR (FR) in GMR/EMT of CRC cells. Finally, CEA/blood glucose (CSR) was defined as a new index, which can be used to jointly diagnose liver metastasis of colorectal cancer.

CONCLUSIONS

GMR in CRC cells is closely associated with the EMT pathway, and this network is a promising source of potential therapeutic targets.

摘要

背景

葡萄糖代谢重编程（GMR）是致癌和转移的一个主要特征。然而，其潜在机制尚未完全阐明。本研究旨在通过整合组学分析，描绘转移性结直肠癌（mCRC）患者原发病灶和循环肿瘤细胞的代谢特征。

方法

分析了 325 例高 18F-氟代脱氧葡萄糖（FDGhigh）mCRC 患者的 PET-CT 成像、血清代谢组学、基因组学和蛋白质组学数据。使用 mCRC 患者的癌旁组织、原发肿瘤和肝转移组织进行蛋白质组学分析。

结果

PET/CT 图像显示肿瘤组织的葡萄糖摄取与血清谷氨酸-丙酮酸转氨酶（ALT）、总胆红素（TBIL）、肌酐（CRE）水平相关。蛋白质组学分析表明，GMR 和上皮-间充质转化（EMT）相关途径中富集了几个差异表达的蛋白。使用组织优化的蛋白质组学工作流程，我们鉴定了新的蛋白质组学标志物（如 CCND1、EPCAM、RPS6）、一个新的 PCK1-CDK6-INSR 蛋白轴，以及 FR 在 CRC 细胞的 GMR/EMT 中的潜在作用。最后，定义 CEA/血糖（CSR）为新的指标，可用于联合诊断结直肠癌肝转移。

结论

CRC 细胞中的 GMR 与 EMT 途径密切相关，该网络是潜在治疗靶点的有希望来源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/fb52f8c60946/fimmu-14-1179699-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/ac0e94bd64ad/fimmu-14-1179699-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/6fca3b28b44b/fimmu-14-1179699-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/c5595fd60040/fimmu-14-1179699-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/77445049483f/fimmu-14-1179699-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/fd3096c4b752/fimmu-14-1179699-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/861a033d047c/fimmu-14-1179699-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/fb52f8c60946/fimmu-14-1179699-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/ac0e94bd64ad/fimmu-14-1179699-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/6fca3b28b44b/fimmu-14-1179699-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/c5595fd60040/fimmu-14-1179699-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/77445049483f/fimmu-14-1179699-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/fd3096c4b752/fimmu-14-1179699-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/861a033d047c/fimmu-14-1179699-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c04/10354426/fb52f8c60946/fimmu-14-1179699-g007.jpg

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