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代谢途径作为胰腺导管腺癌的一种新视野

Metabolic Pathways as a Novel Landscape in Pancreatic Ductal Adenocarcinoma.

作者信息

Ali Ahmad, Chianese Ugo, Papulino Chiara, Toraldo Antonella, Abakar Mawada Elmagboul Abdalla, Passaro Eugenia, Cennamo Rosario, Del Gaudio Nunzio, Altucci Lucia, Benedetti Rosaria

机构信息

Department of Precision Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.

AORN Chirurgia d'Urgenza, Ospedale Cardarelli, 80131 Naples, Italy.

出版信息

Cancers (Basel). 2022 Aug 4;14(15):3799. doi: 10.3390/cancers14153799.

DOI:10.3390/cancers14153799
PMID:35954462
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9367608/
Abstract

Metabolism plays a fundamental role in both human physiology and pathology, including pancreatic ductal adenocarcinoma (PDAC) and other tumors. Anabolic and catabolic processes do not only have energetic implications but are tightly associated with other cellular activities, such as DNA duplication, redox reactions, and cell homeostasis. PDAC displays a marked metabolic phenotype and the observed reduction in tumor growth induced by calorie restriction with in vivo models supports the crucial role of metabolism in this cancer type. The aggressiveness of PDAC might, therefore, be reduced by interventions on bioenergetic circuits. In this review, we describe the main metabolic mechanisms involved in PDAC growth and the biological features that may favor its onset and progression within an immunometabolic context. We also discuss the need to bridge the gap between basic research and clinical practice in order to offer alternative therapeutic approaches for PDAC patients in the more immediate future.

摘要

新陈代谢在人类生理学和病理学中都起着基础性作用,包括胰腺导管腺癌(PDAC)和其他肿瘤。合成代谢和分解代谢过程不仅具有能量方面的影响,还与其他细胞活动紧密相关,如DNA复制、氧化还原反应和细胞稳态。PDAC表现出显著的代谢表型,体内模型中观察到的热量限制诱导的肿瘤生长减缓支持了新陈代谢在这种癌症类型中的关键作用。因此,通过对生物能量回路的干预可能会降低PDAC的侵袭性。在这篇综述中,我们描述了参与PDAC生长的主要代谢机制以及在免疫代谢背景下可能有利于其发生和发展的生物学特征。我们还讨论了弥合基础研究与临床实践之间差距的必要性,以便在不久的将来为PDAC患者提供替代治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2478/9367608/79a92d573606/cancers-14-03799-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2478/9367608/f8ad027d57cf/cancers-14-03799-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2478/9367608/9ca3d4e2e54d/cancers-14-03799-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2478/9367608/79a92d573606/cancers-14-03799-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2478/9367608/f8ad027d57cf/cancers-14-03799-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2478/9367608/9ca3d4e2e54d/cancers-14-03799-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2478/9367608/79a92d573606/cancers-14-03799-g003.jpg

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iScience. 2022 May 30;25(6):104483. doi: 10.1016/j.isci.2022.104483. eCollection 2022 Jun 17.
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USP25 promotes pathological HIF-1-driven metabolic reprogramming and is a potential therapeutic target in pancreatic cancer.USP25 促进病理性 HIF-1 驱动的代谢重编程,是胰腺癌的一个潜在治疗靶点。
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Enhanced pentose phosphate pathway activity promotes pancreatic ductal adenocarcinoma progression via activating YAP/MMP1 axis under chronic acidosis.
重塑胰腺癌肿瘤微环境:转移抑制因子NDRG1的新作用
Cancers (Basel). 2023 May 16;15(10):2779. doi: 10.3390/cancers15102779.
增强的戊糖磷酸途径活性通过在慢性酸中毒下激活 YAP/MMP1 轴促进胰腺导管腺癌的进展。
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Lipid Droplet-Related PLIN2 in CD68 Tumor-Associated Macrophage of Oral Squamous Cell Carcinoma: Implications for Cancer Prognosis and Immunotherapy.口腔鳞状细胞癌CD68肿瘤相关巨噬细胞中与脂滴相关的PLIN2:对癌症预后和免疫治疗的意义
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Autophagy Contributes to Metabolic Reprogramming and Therapeutic Resistance in Pancreatic Tumors.自噬有助于代谢重编程和胰腺肿瘤的治疗抵抗。
Cells. 2022 Jan 26;11(3):426. doi: 10.3390/cells11030426.
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