Cancer-Associated Fibroblasts Autophagy Enhances Progression of Triple-Negative Breast Cancer Cells

Wang, Mengchuan; Zhang, Jian; Huang, Yi-Zhe; Ji, Shufeng; Shao, Guoli; Feng, Shiyu; Chen, Danxun; Zhao, Kankan; Wang, Zixiang; Wu, Aiguo

doi:10.12659/msm.902870

Cited by 54 publications

(49 citation statements)

References 34 publications

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“…Treatment with autophagy target Vps34 inhibitor, SAR405, attenuated xenograft growth and inhibited the effects of standard therapy [28]. Similar results were found both in vitro (co-cultured model) or in vivo (xenografted model and clinical tissue) in cancer researches such as breast cancer, ovarian cancer, liver cancer, colorectal cancer and pancreatic adenocarcinoma [29, 30]. Additionally, there is extensive evidence in literature demonstrating that both radiation and chemotherapeutic drugs promote cytoprotective autophagy in tumor cells.…”

Section: Introductionmentioning

confidence: 65%

The effects and the mechanisms of autophagy on the cancer-associated fibroblasts in cancer

Yan

Chen

Wang

et al. 2019

J Exp Clin Cancer Res

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Cancer-associated fibroblasts (CAFs) plays an essential role in cancer cell growth, metabolism and immunoreaction. Autophagy is an intracellular self-degradative process that balances cell energy source and regulates tissue homeostasis. Targeting autophagy has gained interest with multiple preclinical and clinical trials, such as the pharmacological inhibitor chloroquine or the inducer rapamycin, especially in exploiting its ability to modulate the secretory capability of CAFs to enhance drug delivery or inhibit it to prevent its influence on cancer cell chemoresistance. In this review, we summarize the reports on autophagy in cancer-associated fibroblasts by detailing the mechanism and role of autophagy in CAFs, including the hypoxic-autophagy positive feedback cycle, the metabolic cross-talk between CAFs and tumors induced by autophagy, CAFs secreted cytokines promote cancer survival by secretory autophagy, CAFs autophagy-induced EMT, stemness, senescence and treatment sensitivity, as well as the research of antitumor chemicals, miRNAs and lncRNAs. Additionally, we discuss the evidence of molecules in CAFs that are relevant to autophagy and the contribution to sensitive treatments as a potential target for cancer treatment.

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Section: Introductionmentioning

confidence: 65%

The effects and the mechanisms of autophagy on the cancer-associated fibroblasts in cancer

Yan

Chen

Wang

et al. 2019

J Exp Clin Cancer Res

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“…Notably, we observe reductions in IL6, CXCL8, CXCL1/GROa (C-X-C motif chemokine ligand 1), and LIF/leukemia inhibitory factor (LIF interleukin 6 family cytokine) following BECN1 knockdown in cancer-associated fibroblasts (CAFs) [34]. In breast cancer, CAFs have increased autophagy relative to normal fibroblasts [58]. Conditioned media collected from cancer-associated fibroblasts promotes cancer migration, whereas autophagy inhibition in cancer-associated fibroblasts using 3-MA diminishes cancer migration [58].…”

Section: Cancermentioning

confidence: 89%

“…In breast cancer, CAFs have increased autophagy relative to normal fibroblasts [58]. Conditioned media collected from cancer-associated fibroblasts promotes cancer migration, whereas autophagy inhibition in cancer-associated fibroblasts using 3-MA diminishes cancer migration [58]. Additionally, HMGB1 secreted by autophagydependent secretion in CAFs promotes the maintenance of breast cancer stem cells [59].…”

Section: Cancermentioning

confidence: 99%

Autophagy-dependent secretion: mechanism, factors secreted, and disease implications

2019

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Although best understood as a degradative pathway, recent evidence demonstrates pronounced involvement of the macroautophagic/autophagic molecular machinery in cellular secretion. With either overexpression or inhibition of autophagy mediators, dramatic alterations in the cellular secretory profile occur. This affects secretion of a plethora of factors ranging from cytokines, to granule contents, and even viral particles. Encompassing a wide range of secreted factors, autophagy-dependent secretion is implicated in diseases ranging from cancer to neurodegeneration. With a growing body of evidence shedding light onto the molecular mediators, this review delineates the molecular machinery involved in selective targeting of the autophagosome for either degradation or secretion. In addition, we summarize the current understanding of factors and cargo secreted through this unconventional route, and describe the implications of this pathway in both health and disease.

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“…In LVI, podoplanin positivity is more frequent than CD31 or CD34 positivity and is associated with the development of nodal metastasis and poor clinical outcome [29, 46]. CAFs are also a major source of N-cadherin in BC, thus affecting the tumour cells’ migration by prompting them to leave the primary site and start the migration process [47]. Furthermore, stromal fibroblast transformation into CAFs could be promoted through the loss of interleukin (IL)-6, hence promoting BC cell migration and invasion [48].…”

Section: Interaction With the Surrounding Microenvironmentmentioning

confidence: 99%

Molecular Complexity of Lymphovascular Invasion: The Role of Cell Migration in Breast Cancer as a Prototype

et al. 2020

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Lymphovascular invasion (LVI) is associated with poor outcome in breast cancer (BC); however, its underlying mechanisms remain ill-defined. LVI in BC develops through complex molecular pathways involving not only the interplay with the surrounding microenvironment along with endothelial cells lining the lymphovascular spaces but also changes in the malignant epithelial cells with the acquisition of more invasive and migration abilities. In this review, we focus on the key features that enable tumour cell detachment from the primary niche, their migration and interaction with the surrounding microenvironment as well as the crosstalk with the vascular endothelial cells, which eventually lead to intravasation of tumour cells and LVI. Intravascular tumour cell survival and migration, their distant site extravasation, stromal invasion and growth are part of the metastatic cascade. Cancer cell migration commences with loss of tumour cells' cohesion initiating the invasion and migration processes which are usually accompanied by the accumulation of specific cellular and molecular changes that enable tumour cells to overcome the blockades of the extracellular matrix, spread into surrounding tissues and interact with stromal cells and immune cells. Thereafter, tumour cells migrate further via interacting with lymphovascular endothelial cells to penetrate the vessel wall leading ultimately to intravasation of cancer cells. Exploring the potential factors influencing cell migration in LVI can help in understanding the underlying mechanisms of LVI to identify targeted therapy in BC.

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Cancer-Associated Fibroblasts Autophagy Enhances Progression of Triple-Negative Breast Cancer Cells

Cited by 54 publications

References 34 publications

The effects and the mechanisms of autophagy on the cancer-associated fibroblasts in cancer

The effects and the mechanisms of autophagy on the cancer-associated fibroblasts in cancer

Autophagy-dependent secretion: mechanism, factors secreted, and disease implications

Molecular Complexity of Lymphovascular Invasion: The Role of Cell Migration in Breast Cancer as a Prototype

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