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休眠促进肿瘤复发。

When dormancy fuels tumour relapse.

机构信息

Molecular Oncology Programme, Growth Factors, Nutrients and Cancer Group, Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain.

出版信息

Commun Biol. 2021 Jun 16;4(1):747. doi: 10.1038/s42003-021-02257-0.


DOI:10.1038/s42003-021-02257-0
PMID:34135460
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8209066/
Abstract

Tumour recurrence is a serious impediment to cancer treatment, but the mechanisms involved are poorly understood. The most frequently used anti-tumour therapies-chemotherapy and radiotherapy-target highly proliferative cancer cells. However non- or slow-proliferative dormant cancer cells can persist after treatment, eventually causing tumour relapse. Whereas the reversible growth arrest mechanism allows quiescent cells to re-enter the cell cycle, senescent cells are largely thought to be irreversibly arrested, and may instead contribute to tumour growth and relapse through paracrine signalling mechanisms. Thus, due to the differences in their growth arrest mechanism, metabolic features, plasticity and adaptation to their respective tumour microenvironment, dormant-senescent and -quiescent cancer cells could have different but complementary roles in fuelling tumour growth. In this review article, we discuss the implication of dormant cancer cells in tumour relapse and the need to understand how quiescent and senescent cells, respectively, may play a part in this process.

摘要

肿瘤复发是癌症治疗的严重障碍,但其中涉及的机制尚不清楚。最常使用的抗肿瘤疗法——化疗和放疗——针对高度增殖的癌细胞。然而,非增殖或缓慢增殖的休眠癌细胞在治疗后可能仍然存在,最终导致肿瘤复发。虽然可逆的生长停滞机制允许静止细胞重新进入细胞周期,但衰老细胞被认为是不可逆的停滞,可能通过旁分泌信号机制促进肿瘤生长和复发。因此,由于它们的生长停滞机制、代谢特征、可塑性以及对各自肿瘤微环境的适应能力不同,休眠-衰老和静止癌细胞在促进肿瘤生长方面可能具有不同但互补的作用。在这篇综述文章中,我们讨论了休眠癌细胞在肿瘤复发中的意义,以及需要了解静止细胞和衰老细胞分别在这一过程中可能起到的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d210/8209066/efa79842e51f/42003_2021_2257_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d210/8209066/26529f97261f/42003_2021_2257_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d210/8209066/6da3ebdce257/42003_2021_2257_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d210/8209066/efa79842e51f/42003_2021_2257_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d210/8209066/26529f97261f/42003_2021_2257_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d210/8209066/6da3ebdce257/42003_2021_2257_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d210/8209066/efa79842e51f/42003_2021_2257_Fig3_HTML.jpg

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本文引用的文献

[1]
Colorectal Cancer Cells Enter a Diapause-like DTP State to Survive Chemotherapy.

Cell. 2021-1-7

[2]
An Embryonic Diapause-like Adaptation with Suppressed Myc Activity Enables Tumor Treatment Persistence.

Cancer Cell. 2021-2-8

[3]
Single-cell landscape of the ecosystem in early-relapse hepatocellular carcinoma.

Cell. 2021-1-21

[4]
Adaptive T-cell immunity controls senescence-prone MyD88- or CARD11-mutant B-cell lymphomas.

Blood. 2021-5-20

[5]
G3BP1 controls the senescence-associated secretome and its impact on cancer progression.

Nat Commun. 2020-10-5

[6]
Senolytic CAR T cells reverse senescence-associated pathologies.

Nature. 2020-6-17

[7]
The force awakens: metastatic dormant cancer cells.

Exp Mol Med. 2020-4

[8]
Senescence-Induced Vascular Remodeling Creates Therapeutic Vulnerabilities in Pancreas Cancer.

Cell. 2020-3-31

[9]
NFATC4 promotes quiescence and chemotherapy resistance in ovarian cancer.

JCI Insight. 2020-4-9

[10]
CDK4/6 Inhibitors Impair Recovery from Cytotoxic Chemotherapy in Pancreatic Adenocarcinoma.

Cancer Cell. 2020-2-27

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