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前列腺癌的代谢适应。

Metabolic adaptations in prostate cancer.

机构信息

Center for Cooperative Research in Biosciences (CIC bioGUNE), Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160, Derio, Spain.

Centro de Investigación Biomédica En Red de Cáncer (CIBERONC), 28029, Madrid, Spain.

出版信息

Br J Cancer. 2024 Nov;131(8):1250-1262. doi: 10.1038/s41416-024-02762-z. Epub 2024 Jul 5.


DOI:10.1038/s41416-024-02762-z
PMID:38969865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11473656/
Abstract

Prostate cancer is one of the most commonly diagnosed cancers in men and is a major cause of cancer-related deaths worldwide. Among the molecular processes that contribute to this disease, the weight of metabolism has been placed under the limelight in recent years. Tumours exhibit metabolic adaptations to comply with their biosynthetic needs. However, metabolites also play an important role in supporting cell survival in challenging environments or remodelling the tumour microenvironment, thus being recognized as a hallmark in cancer. Prostate cancer is uniquely driven by androgen receptor signalling, and this knowledge has also influenced the paths of cancer metabolism research. This review provides a comprehensive perspective on the metabolic adaptations that support prostate cancer progression beyond androgen signalling, with a particular focus on tumour cell intrinsic and extrinsic pathways.

摘要

前列腺癌是男性最常见的癌症之一,也是全球癌症相关死亡的主要原因。在导致这种疾病的分子过程中,近年来代谢的重要性受到了关注。肿瘤表现出代谢适应来满足其生物合成需求。然而,代谢物在支持细胞在挑战性环境中存活或重塑肿瘤微环境方面也发挥着重要作用,因此被认为是癌症的一个标志。前列腺癌是由雄激素受体信号驱动的,这一知识也影响了癌症代谢研究的方向。本文综述了除雄激素信号外支持前列腺癌进展的代谢适应,特别关注肿瘤细胞内在和外在途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/7a55a93356ea/41416_2024_2762_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/cd078fd7ebca/41416_2024_2762_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/3796eebf0e63/41416_2024_2762_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/faac5a686f17/41416_2024_2762_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/7a55a93356ea/41416_2024_2762_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/cd078fd7ebca/41416_2024_2762_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/3796eebf0e63/41416_2024_2762_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/faac5a686f17/41416_2024_2762_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d231/11473656/7a55a93356ea/41416_2024_2762_Fig4_HTML.jpg

相似文献

[1]
Metabolic adaptations in prostate cancer.

Br J Cancer. 2024-11

[2]
A review on the interactions between the tumor microenvironment and androgen receptor signaling in prostate cancer.

Transl Res. 2018-11-24

[3]
Intracellular adaptor molecules and AR signalling in the tumour microenvironment.

Cell Signal. 2010-12-3

[4]
Tumour metabolism and its unique properties in prostate adenocarcinoma.

Nat Rev Urol. 2020-2-28

[5]
Stromal androgen receptor regulates the composition of the microenvironment to influence prostate cancer outcome.

Oncotarget. 2015-6-30

[6]
Prostate cancer: Re-focusing on androgen receptor signaling.

Int J Biochem Cell Biol. 2007

[7]
Regulation of Molecular Biomarkers Associated with the Progression of Prostate Cancer.

Int J Mol Sci. 2024-4-10

[8]
Androgens regulate prostate cancer cell growth via an AMPK-PGC-1α-mediated metabolic switch.

Oncogene. 2014-11-6

[9]
Cancer Cell-Extrinsic Roles for the Androgen Receptor in Prostate Cancer.

Endocrinology. 2023-4-17

[10]
[The mechanism of progression without androgen receptor interaction in prostate cancer].

Nihon Rinsho. 2016-1

引用本文的文献

[1]
The Oncometabolite 2-Hydroxyglutarate Is Upregulated in Post-Prostatectomy PSA Recurrence of Prostate Cancer: A Metabolomic Analysis.

Molecules. 2025-8-8

[2]
New frontiers in prostate cancer treatment from systemic therapy to targeted therapy.

EMBO Mol Med. 2025-8-4

[3]
Urinary Extracellular Vesicle Signatures as Biomarkers in Prostate Cancer Patients.

Int J Mol Sci. 2025-7-18

[4]
Steroid Sulfatase Regulates Metabolic Reprogramming in Advanced Prostate Cancer.

Cancers (Basel). 2025-6-12

[5]
Role of Tumor Microenvironment in Prostate Cancer Immunometabolism.

Biomolecules. 2025-6-6

[6]
Development and validation of tryptophan metabolism-related risk model and molecular subtypes for predicting postoperative biochemical recurrence in prostate cancer.

Transl Androl Urol. 2025-4-30

[7]
Inhibition of Mitochondrial-Associated Protein MAGMAS Resensitizes Chemoresistant Prostate Cancer Cells to Docetaxel.

Cancers (Basel). 2025-4-30

[8]
Poloxamer-based drug delivery systems: Frontiers for treatment of solid tumors.

Mater Today Bio. 2025-4-2

[9]
Transcriptomic signatures of prostate cancer progression: a comprehensive RNA-seq study.

3 Biotech. 2025-5

[10]
CellPie: a scalable spatial transcriptomics factor discovery method via joint non-negative matrix factorization.

Nucleic Acids Res. 2025-3-20

本文引用的文献

[1]
FABP5 Inhibition against -Mutant Therapy Resistant Prostate Cancer.

Cancers (Basel). 2023-12-21

[2]
Prostate lineage-specific metabolism governs luminal differentiation and response to antiandrogen treatment.

Nat Cell Biol. 2023-12

[3]
Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity.

Cancer Res. 2024-3-4

[4]
CD36 maintains lipid homeostasis via selective uptake of monounsaturated fatty acids during matrix detachment and tumor progression.

Cell Metab. 2023-11-7

[5]
MYC is a regulator of androgen receptor inhibition-induced metabolic requirements in prostate cancer.

Cell Rep. 2023-10-31

[6]
Fatty acid binding protein 5 regulates docetaxel sensitivity in taxane-resistant prostate cancer cells.

PLoS One. 2023

[7]
Formate Supplementation Enhances Antitumor CD8+ T-cell Fitness and Efficacy of PD-1 Blockade.

Cancer Discov. 2023-12-12

[8]
Rescue of dendritic cells from glycolysis inhibition improves cancer immunotherapy in mice.

Nat Commun. 2023-9-2

[9]
MBTPS2 acts as a regulator of lipogenesis and cholesterol synthesis through SREBP signalling in prostate cancer.

Br J Cancer. 2023-6

[10]
The evolving tumor microenvironment: From cancer initiation to metastatic outgrowth.

Cancer Cell. 2023-3-13

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