Fibroblast growth factors signaling in bone metastasis

Labanca, Estefanía; Vázquez, Elba S.; Corn, Paul G.; Roberts, Justin; Wang, Fen; Logothetis, Christopher J.; Navone, Nora M.

doi:10.1530/erc-19-0472

Cited by 22 publications

(17 citation statements)

References 74 publications

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“…bFGF (also known as FGF-2 or FGF-β) was not only an identified angiogenic cytokine ( 73 ), but also implicated in tumor maintenance and metastasis ( 74 ). bFGF was identified as a mediator to protect auditory neurons from acoustic trauma and aminoglycoside ototoxicity, it was 3.5-fold higher in good hearing VS versus poor hearing VS ( 75 ), and its plasma concentration increased while patient’s hearing improved after bevacizumab regimen ( 76 ).…”

Section: Resultsmentioning

confidence: 99%

Potential Molecular Biomarkers of Vestibular Schwannoma Growth: Progress and Prospects

et al. 2021

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Vestibular schwannomas (VSs, also known as acoustic neuromas) are relatively rare benign brain tumors stem from the Schwann cells of the eighth cranial nerve. Tumor growth is the paramount factor for neurosurgeons to decide whether to choose aggressive treatment approach or careful follow-up with regular magnetic resonance imaging (MRI), as surgery and radiation can introduce significant trauma and affect neurological function, while tumor enlargement during long-term follow-up will compress the adjacent nerves and tissues, causing progressive hearing loss, tinnitus and vertigo. Recently, with the deepening research of VS biology, some proteins that regulate merlin conformation changes, inflammatory cytokines, miRNAs, tissue proteins and cerebrospinal fluid (CSF) components have been proposed to be closely related to tumor volume increase. In this review, we discuss advances in the study of biomarkers that associated with VS growth, providing a reference for exploring the growth course of VS and determining the optimal treatment strategy for each patient.

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Section: Resultsmentioning

confidence: 99%

Potential Molecular Biomarkers of Vestibular Schwannoma Growth: Progress and Prospects

et al. 2021

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“…When PC cells localize the bone marrow, the mutual effect between the cancer cells and the microenvironment of bone leads to a bad circle of the destruction and regeneration of bone, a process which supports the survival of cancer cells and the growth of tumors [ 23 – 25 ]. PC cells secrete growth factors, including adrenomedullin, endothelin 1, bone morphogenetic proteins, fibroblast growth factors, and platelet-derived growth factor (PDGF), which can stimulate osteoblasts to activate and form new bone by paracrine signals [ 26 ]. In addition, protease secreted by tumor (urokinase-type plasminogen activator, prostate-specific antigen (PSA), and matrix metalloproteinases) promotes the release of osteoblast-induced growth factors, such as insulin-like growth factors, PDGF, and transforming growth factor β (TGF-β), which further enhances the differentiation of mesenchymal stem cells into osteoblasts [ 27 ].…”

Section: Metastasis Of Pcmentioning

confidence: 99%

Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer

Wang

Jiang

2021

Cell Death Dis

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Prostate cancer is a common malignant tumor, which can spread to multiple organs in the body. Metastatic disease is the dominant reason of death for patients with prostate cancer. Prostate cancer usually transfers to bone. Bone metastases are related to pathologic fracture, pain, and reduced survival. There are many known targets for prostate cancer treatment, including androgen receptor (AR) axis, but drug resistance and metastasis eventually develop in advanced disease, suggesting the necessity to better understand the resistance mechanisms and consider multi-target medical treatment. Because of the limitations of approved treatments, further research into other potential targets is necessary. Metastasis is an important marker of cancer development, involving numerous factors, such as AKT, EMT, ECM, tumor angiogenesis, the development of inflammatory tumor microenvironment, and defect in programmed cell death. In tumor metastasis, programmed cell death (autophagy, apoptosis, and necroptosis) plays a key role. Malignant cancer cells have to overcome the different forms of cell death to transfer. The article sums up the recent studies on the mechanism of bone metastasis involving key regulatory factors such as macrophages and AKT and further discusses as to how regulating autophagy is crucial in relieving prostate cancer bone metastasis.

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“…To further understand metabolic changes that occur during progression we performed a metabolomics analyses in a well-established PDXs that mimic donor response to ADT in a well-controlled study, which is difficult to achieve with clinical samples. The MDA PCa models have already provided unique insights into the biology of PCa (16), including the discovery of: distinct classes of chromosomal rearrangements in PCa cells (24); new therapeutic approaches for combination therapy targeting DNA damage response genes (25, 26); new biological roles of genes in PCa (27); new mechanisms underlying neuroendocrine differentiation (28); molecular alterations commonly found in aggressive variant PCa (29); fibroblast growth factor (FGF) axis in the pathogenesis of PCa bone metastasis (11, 14, 30, 31).…”

Section: Discussionmentioning

confidence: 99%

Prostate cancer castrate resistant progression usage of non-canonical androgen receptor signaling and ketone body fuel

Labanca

Bizzotto

Sanchis

et al. 2021

Preprint

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Prostate cancer (PCa) that progresses after androgen deprivation therapy (ADT) remains incurable. The intricacy of metabolic pathways associated with PCa progression spurred us to develop a metabolism-centric analysis. Using PCa patient-derived xenografts (PDXs) we assessed the metabolic changes after castration of tumor-bearing mice. We found that relapsed tumors had a significant increase in fatty acids and ketone body content compared with baseline. We confirmed that critical ketogenic/ketolytic enzymes (ACAT1, OXCT1, BDH1) were significantly augmented after castrate-resistant progression. Further, these enzymes are increased in the human donor tissue after progressing to ADT.Increased ACAT1 and OXCT1 was also observed for a subset of PCa patients that relapsed with low AR and ERG expression. These factors were associated with decreased biochemical relapse and progression free survival. In summary, our studies reveal the key metabolites fueling castration resistant progression in the context of a partial or complete loss of AR dependence.

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Fibroblast growth factors signaling in bone metastasis

Cited by 22 publications

References 74 publications

Potential Molecular Biomarkers of Vestibular Schwannoma Growth: Progress and Prospects

Potential Molecular Biomarkers of Vestibular Schwannoma Growth: Progress and Prospects

Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer

Prostate cancer castrate resistant progression usage of non-canonical androgen receptor signaling and ketone body fuel

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