Cancer-associated fibroblasts promote malignant phenotypes of prostate cancer cells via autophagy :  Cancer-associated fibroblasts promote prostate cancer development

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Abstract

Dysregulation of autophagy in cancer-associated fibroblasts (CAFs) has been demonstrated to play a role in malignant phenotypes of human tumors. We intended to investigate the function of CAFs autophagy in prostate cancer (PCa). Firstly, CAFs and normal fibroblasts (NFs) were isolated from cancerous and adjacent normal tissues of PCa patients, for the following experimental preparation. In comparison with NFs, CAFs expressed higher levels of the myofibroblast marker ?-smooth muscle actin (?-SMA) and the mesenchymal marker Vimentin. Besides, CAFs possessed a higher autophagic level than NFs. As for malignant phenotypes, PCa cells co-cultured with CAFs-CM showed greater proliferation, migration and invasion capabilities, while these outcomes were obviously abolished by autophagy inhibition with 3-Methyladenine (3-MA). Moreover, silencing of ATG5 in CAFs inhibited fibroblasts autophagic level and suppressed malignant phenotypes of PCa cells, while ATG5 overexpression in NFs exerted opposite effects. Depletion of ATG5 in CAFs inhibited the xenograft tumor growth and lung metastasis of PCa cells. Taken together, our data demonstrated the promotive effect of CAFs on PCa malignant phenotypes through ATG5-dependent autophagy, suggesting a novel mechanism for PCa progression.

Supplementary Information

The online version contains supplementary material available at 10.1007/s10495-023-01828-2.

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Most cited references 39

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Cancer statistics, 2020

Rebecca Siegel, Kimberly D Miller, Ahmedin Jemal (2020)

Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States and compiles the most recent data on population-based cancer occurrence. Incidence data (through 2016) were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data (through 2017) were collected by the National Center for Health Statistics. In 2020, 1,806,590 new cancer cases and 606,520 cancer deaths are projected to occur in the United States. The cancer death rate rose until 1991, then fell continuously through 2017, resulting in an overall decline of 29% that translates into an estimated 2.9 million fewer cancer deaths than would have occurred if peak rates had persisted. This progress is driven by long-term declines in death rates for the 4 leading cancers (lung, colorectal, breast, prostate); however, over the past decade (2008-2017), reductions slowed for female breast and colorectal cancers, and halted for prostate cancer. In contrast, declines accelerated for lung cancer, from 3% annually during 2008 through 2013 to 5% during 2013 through 2017 in men and from 2% to almost 4% in women, spurring the largest ever single-year drop in overall cancer mortality of 2.2% from 2016 to 2017. Yet lung cancer still caused more deaths in 2017 than breast, prostate, colorectal, and brain cancers combined. Recent mortality declines were also dramatic for melanoma of the skin in the wake of US Food and Drug Administration approval of new therapies for metastatic disease, escalating to 7% annually during 2013 through 2017 from 1% during 2006 through 2010 in men and women aged 50 to 64 years and from 2% to 3% in those aged 20 to 49 years; annual declines of 5% to 6% in individuals aged 65 years and older are particularly striking because rates in this age group were increasing prior to 2013. It is also notable that long-term rapid increases in liver cancer mortality have attenuated in women and stabilized in men. In summary, slowing momentum for some cancers amenable to early detection is juxtaposed with notable gains for other common cancers.

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A framework for advancing our understanding of cancer-associated fibroblasts

Erik Sahai, Igor Astsaturov, Edna Cukierman … (2020)

Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with diverse functions, including matrix deposition and remodelling, extensive reciprocal signalling interactions with cancer cells and crosstalk with infiltrating leukocytes. As such, they are a potential target for optimizing therapeutic strategies against cancer. However, many challenges are present in ongoing attempts to modulate CAFs for therapeutic benefit. These include limitations in our understanding of the origin of CAFs and heterogeneity in CAF function, with it being desirable to retain some antitumorigenic functions. On the basis of a meeting of experts in the field of CAF biology, we summarize in this Consensus Statement our current knowledge and present a framework for advancing our understanding of this critical cell type within the tumour microenvironment.

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Biological Functions of Autophagy Genes: A Disease Perspective

Beth Levine, Guido Kroemer (2019)

The lysosomal degradation pathway of autophagy plays a fundamental role in cellular, tissue, and organismal homeostasis and is mediated by evolutionarily conserved autophagy-related (ATG) genes. Definitive etiological links exist between mutations in genes that control autophagy and human disease, especially neurodegenerative, inflammatory disorders and cancer. Autophagy selectively targets dysfunctional organelles, intracellular microbes, and pathogenic proteins, and deficiencies in these processes may lead to disease. Moreover, ATG genes have diverse physiologically important roles in other membrane-trafficking and signaling pathways. This Review discusses the biological functions of autophagy genes from the perspective of understanding-and potentially reversing-the pathophysiology of human disease and aging.

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Author and article information

Contributors

YuanGuang Zhang: zhangyguangz1220@163.com

Pan Liu: liupan85@126.com

Journal

Journal ID (nlm-ta): Apoptosis

Journal ID (iso-abbrev): Apoptosis

Title: Apoptosis

Publisher: Springer US (New York )

ISSN (Print): 1360-8185

ISSN (Electronic): 1573-675X

Publication date (Electronic): 31 March 2023

Publication date PMC-release: 31 March 2023

Publication date (Print): 2023

Volume: 28

Issue: 5-6

Pages: 881-891

Affiliations

[1 ]GRID grid.501248.a, Department of Neurosurgery, , Zhuzhou Central Hospital, ; Zhuzhou, Hunan Province 412007 P.R. China

[2 ]GRID grid.501248.a, Department of Orthopaedics, , Zhuzhou Central Hospital, ; Zhuzhou, Hunan Province 412007 P.R. China

[3 ]GRID grid.501248.a, Department of Trauma Center, , Zhuzhou Central Hospital, ; Zhuzhou, Hunan Province 412007 P.R. China

[4 ]GRID grid.501248.a, Department of Urology, , Zhuzhou Central Hospital, ; Zhuzhou, Hunan Province 412007 P.R. China

[5 ]GRID grid.501248.a, Department of Spine surgery, , Zhuzhou Central Hospital, ; No. 116, Changjiang South Road, Tianyuan District, Zhuzhou, Hunan Province 412007 P.R. China

[6 ]GRID grid.501248.a, Department of Emergency, , Zhuzhou Central Hospital, ; No. 116, Changjiang South Road, Tianyuan District, Zhuzhou, Hunan Province 412007 P.R. China

Article

Publisher ID: 1828

DOI: 10.1007/s10495-023-01828-2

PMC ID: 10232635

PubMed ID: 37000314

SO-VID: 32db58a7-c19f-4faf-bee5-aad1a451de5e

Copyright © © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

History

Date accepted : 5 March 2023

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ScienceOpen disciplines: Molecular biology

Keywords: cancer-associated fibroblasts,atg5,autophagy,prostate cancer,malignant phenotype

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ScienceOpen disciplines: Molecular biology

Keywords: cancer-associated fibroblasts, atg5, autophagy, prostate cancer, malignant phenotype

Cancer-associated fibroblasts promote malignant phenotypes of prostate cancer cells via autophagy : Cancer-associated fibroblasts promote prostate cancer development

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Higher order chromatin architecture

Most cited references 39

Cancer statistics, 2020

A framework for advancing our understanding of cancer-associated fibroblasts

Biological Functions of Autophagy Genes: A Disease Perspective

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