FGF19 promotes progression of prostate cancer

Nagamatsu, Hirotaka; Teishima, Jun; Goto, Keisuke; Shikuma, Hiroyuki; Kohno, Hiroyuki; Shoji, Koichi; Inoue, Shogo; Matsubara, Akio

doi:10.1002/pros.22994

Cited by 38 publications

(28 citation statements)

References 24 publications

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“…However, a large body of research has demonstrated that this signaling axis is highly deregulated in numerous cancers, including amplification of FGFs in epithelial or stromal cells, and/or aberrant expression or activation of FGFRs resulting from genetic translocation, mutation, or amplification in tumorigenic cells (2). Pathological FGF/FGFRs signaling promotes crosstalk of tumorigenic cells with their microenvironment, which drives tumor proliferation, angiogenesis, and metastasis in cancer progression (3)(4)(5)(6)(7)(8).…”

Section: Discussionmentioning

confidence: 99%

Pharmacologically targeting the myristoylation of the scaffold protein FRS2α inhibits FGF/FGFR-mediated oncogenic signaling and tumor progression

Li¹,

Alsaidan²,

Ma³

et al. 2018

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Pharmacologically targeting the myristoylation of the scaffold protein FRS2α inhibits FGF/FGFR-mediated oncogenic signaling and tumor progression

Li¹,

Alsaidan²,

Ma³

et al. 2018

Journal of Biological Chemistry

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“…Recently, amplification of the FGF19 gene has been identified as a frequent genetic aberration in HCC, prostate, breast, and lung squamous cancers . However, the clinical correlation of FGF19 gene amplification and the potential therapeutic effects of targeting FGF19 in LSCC are not yet clear.…”

Section: Discussionmentioning

confidence: 99%

FGF19 genetic amplification as a potential therapeutic target in lung squamous cell carcinomas

et al. 2017

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BackgroundAlthough FGF 19 gene aberrations are associated with carcinogenesis and progression in human cancers, the roles of FGF 19 genetic amplification and expression in Chinese patients with lung squamous cell carcinoma (LSCC) and FGF 19 amplification as a potential therapeutic target for LSCC are not well understood.MethodsFluorescence in situ hybridization analysis and quantitative real‐time‐PCR was used to detect FGF 19 genetic amplification and FGF 19 messenger RNA expression in LSCC tumor and paired adjacent samples. Small interfering RNA and short hairpin RNA were used to knockdown FGF19 in vitro and in vivo. Results FGF 19 amplification was identified in a subset of LSCC patients (37.5%, 15/40), and upregulation of FGF 19 expression was found in 60% (24/40) of tumor tissues compared to adjacent non‐tumorous tissues. Correlation analysis with clinicopathologic parameters showed that FGF 19 upregulation was significantly associated with heavy smoking. Small interfering RNA knockdown of FGF 19 led to the significant inhibition of cell growth and induced apoptosis in LSCC cells carrying the amplified FGF 19 gene, but these effects was not observed in non‐amplified LSCC cells. Interfering FGF 19 expression with short hairpin RNA also resulted in tumor growth inhibition and induced apoptosis in LSCC xenografts with amplified FGF 19 in tumor cells.ConclusionOur results suggested that FGF 19 signaling activation is required for cell growth and survival of FGF 19 amplified LSCC cells, both in vitro and in vivo. Intervention of FGF 19 activation could be a potential therapeutic strategy for LSCC patients with FGF 19 amplification.

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“…In addition, engineered forms of FGF19 which retain the ability to regulate bile acid metabolism but lack tumorigenicity have been reported [96,97]. However, induction of FGF19 has also been associated with the development and aggressiveness of other types of cancer including prostate [98,99] and colon cancer [100]. Therapeutic strategies to inhibit FGF19 function to reduce cancer progression have been proposed and should also be carefully evaluated.…”

Section: Metabolic Actions Of Fgf15/19mentioning

confidence: 99%

Metabolic fibroblast growth factors (FGFs): Mediators of energy homeostasis

Markan

Potthoff

2016

Seminars in Cell & Developmental Biology

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The metabolic fibroblast growth factors (FGFs), FGF1, FGF15/19, and FGF21 differ from classic FGFs in that they modulate energy homeostasis in response to fluctuating nutrient availability. These unique mediators of metabolism regulate a number of physiological processes which contribute to their potent pharmacological properties. Administration of pharmacological doses of these FGFs causes weight loss, increases energy expenditure, and improves carbohydrate and lipid metabolism in obese animal models. However, many questions remain regarding the precise molecular and physiological mechanisms governing the effects of individual metabolic FGFs. Here we review the metabolic actions of FGF1, FGF15/19, and FGF21 while providing insights into their pharmacological effects by examining known biological functions.

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FGF19 promotes progression of prostate cancer

Abstract: FGF19 might be associated with biochemical recurrence after radical prostatectomy by promoting cell proliferation and epithelial-mesenchymal transition of PCa.

Cited by 38 publications

References 24 publications

Pharmacologically targeting the myristoylation of the scaffold protein FRS2α inhibits FGF/FGFR-mediated oncogenic signaling and tumor progression

Pharmacologically targeting the myristoylation of the scaffold protein FRS2α inhibits FGF/FGFR-mediated oncogenic signaling and tumor progression

FGF19 genetic amplification as a potential therapeutic target in lung squamous cell carcinomas

Metabolic fibroblast growth factors (FGFs): Mediators of energy homeostasis

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