Fibroblast growth factor‐2, derived from cancer‐associated fibroblasts, stimulates growth and progression of human breast cancer cells via FGFR1 signaling

Suh, Jinyoung; Kim, Do‐Hee; Lee, Yeon‐Hwa; Jang, Ja Young; Surh, Young‐Joon

doi:10.1002/mc.23233

Cited by 52 publications

(37 citation statements)

References 52 publications

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“…Herein, fibroblasts would involve in regulating ECM via synthesizing matrix components, such as collagen, laminin, and fibronectin. [ 26 ] In addition, endothelial cells play a critical role in regulating the survival of whole spheroids. Without HUVEC, even though it succeeded in forming a united spheroid, the red core (dead) fluorescence indicated a hypoxia‐induced necrotic domain (Figure 2c).…”

Section: Resultsmentioning

confidence: 99%

Close to Real: Large‐Volume 3D Cell Spheroids on a Superamphiphobic Surface

Dai

Wang

et al. 2021

Adv Materials Inter

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3D cell spheroids with native cell‐to‐cell junctions and cell‐extracellular matrix interactions can recapitulate the comprehensive physiological environments in vivo, providing new platforms for preclinical drug screening. However, the applications of 3D cell spheroids are limited by the unmatched size, deficient cell abundance, and short service time. In this work, a novel upward culture method on a porous silica superamphiphobic biointerface (SABI) is developed to fully overcome these technical hurdles. Cell suspensions maintain in a state of aquatic marble, accelerating cellular self‐aggregation. Contributing to the upward culture model, this strategy overcomes the shortages of size limitation and media refreshing in the classical methods. Herein, large‐volume 3D cell spheroids with the size of over 1500 µm can be efficiently established within 2 days and subsequently long‐term cultured for more than 20 days. For a close to real biomimetic microenvironment, breast tumor 3D spheroid is applied as a proof of concept, simultaneously employing MCF‐7 cell, cancer‐associated fibroblast (clone 8), and vascular endothelial cell (HUVEC). The large‐volume tumor spheroid with close‐to‐real microenvironment services as a unique paradigm for all‐in‐one biological relevant researches, including the capacity of in situ observation, long‐term incubation, drug screening, and recyclability.

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Section: Resultsmentioning

confidence: 99%

Close to Real: Large‐Volume 3D Cell Spheroids on a Superamphiphobic Surface

Dai

Wang

et al. 2021

Adv Materials Inter

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“…However, this depletion of myeloid lineage cells also led to reductions in CAF number and collagen deposition within end-stage tumors, while macrophage number was not significantly different at end-stage. CAFs have also been implicated in promoting cancer cell proliferation within tumors [84,85]. Although both tumor-associated macrophages and CAFs secrete factors that enhance tumor cell proliferation, the loss of collagen could also significantly impact tumor growth.…”

Section: Discussionmentioning

confidence: 99%

Stromal CCL2 Signaling Promotes Mammary Tumor Fibrosis through Recruitment of Myeloid-Lineage Cells

Kuziel

Thompson

D'Amato

et al. 2020

Cancers

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Obesity is correlated with breast tumor desmoplasia, leading to diminished chemotherapy response and disease-free survival. Obesity causes chronic, macrophage-driven inflammation within breast tissue, initiated by chemokine ligand 2 (CCL2) signaling from adipose stromal cells. To understand how CCL2-induced inflammation alters breast tumor pathology, we transplanted oncogenically transformed human breast epithelial cells with breast stromal cells expressing CCL2 or empty vector into murine mammary glands and examined tumor formation and progression with time. As tumors developed, macrophages were rapidly recruited, followed by the emergence of cancer-associated fibroblasts (CAFs) and collagen deposition. Depletion of CD11b + myeloid lineage cells early in tumor formation reduced tumor growth, CAF numbers, and collagen deposition. CCL2 expression within developing tumors also enhanced recruitment of myeloid progenitor cells from the bone marrow into the tumor site. The myeloid progenitor cell population contained elevated numbers of fibrocytes, which exhibited platelet-derived growth factor receptor-alpha (PDGFRα)-dependent colony formation and growth in vitro. Together, these results suggest that chronic inflammation induced by CCL2 significantly enhances tumor growth and promotes the formation of a desmoplastic stroma through early recruitment of macrophages and fibrocytes into the tumor microenvironment. Fibrocytes may be a novel target in the tumor microenvironment to reduce tumor fibrosis and enhance treatment responses for obese breast cancer patients.

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“…Besides this, the release of FGF7 by CAFs and its interaction with the cognate receptor FGFR2 have been shown to induce ER phosphorylation, ubiquitination, and subsequent proteasomal degradation, therefore counteracting the endocrine treatment in breast cancer cells [ 83 ]. Besides this, the FGF/FGFR axis has been involved in a feedforward stimulatory loop coupling CAFs to breast cancer cells [ 97 , 98 ], whereas the PDGF released by breast tumor cells stimulated the production of FGFs by CAFs towards the activation of proliferative and pro-metastatic pathways in breast cancer cells [ 97 ]. Likewise, the Hedgehog ligand produced by TNBC cells prompted the release of FGF5 by CAFs, leading to the acquisition of a chemo-resistant and cancer stem cell phenotype [ 99 ].…”

Section: The Functional Interplay Between Fgf/fgfr Signaling and Bmentioning

confidence: 99%

The FGF/FGFR System in Breast Cancer: Oncogenic Features and Therapeutic Perspectives

Santolla

Maggiolini

2020

Cancers

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One of the major challenges in the treatment of breast cancer is the heterogeneous nature of the disease. With multiple subtypes of breast cancer identified, there is an unmet clinical need for the development of therapies particularly for the less tractable subtypes. Several transduction mechanisms are involved in the progression of breast cancer, therefore making the assessment of the molecular landscape that characterizes each patient intricate. Over the last decade, numerous studies have focused on the development of tyrosine kinase inhibitors (TKIs) to target the main pathways dysregulated in breast cancer, however their effectiveness is often limited either by resistance to treatments or the appearance of adverse effects. In this context, the fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) system represents an emerging transduction pathway and therapeutic target to be fully investigated among the diverse anti-cancer settings in breast cancer. Here, we have recapitulated previous studies dealing with FGFR molecular aberrations, such as the gene amplification, point mutations, and chromosomal translocations that occur in breast cancer. Furthermore, alterations in the FGF/FGFR signaling across the different subtypes of breast cancer have been described. Next, we discussed the functional interplay between the FGF/FGFR axis and important components of the breast tumor microenvironment. Lastly, we pointed out the therapeutic usefulness of FGF/FGFR inhibitors, as revealed by preclinical and clinical models of breast cancer.

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Fibroblast growth factor‐2, derived from cancer‐associated fibroblasts, stimulates growth and progression of human breast cancer cells via FGFR1 signaling

Cited by 52 publications

References 52 publications

Close to Real: Large‐Volume 3D Cell Spheroids on a Superamphiphobic Surface

Close to Real: Large‐Volume 3D Cell Spheroids on a Superamphiphobic Surface

Stromal CCL2 Signaling Promotes Mammary Tumor Fibrosis through Recruitment of Myeloid-Lineage Cells

The FGF/FGFR System in Breast Cancer: Oncogenic Features and Therapeutic Perspectives

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