Relationship between the localization of fibroblast growth factor 9 in prostate cancer cells and postoperative recurrence

Teishima, Jun; Shoji, Koichi; Hayashi, Tetsutaro; Miyamoto, Kengo; Ohara, Shuichi; Matsubara, Akio

doi:10.1038/pcan.2011.48

Cited by 22 publications

(18 citation statements)

References 25 publications

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“…However, it has also been discovered to facilitate gastric cancer invasion and growth . Besides, FGF9 was believed to indicate a poor prognosis of non‐small‐cell lung cancer, colon cancer, and prostate cancer . However, we found that FGF9 was underexpressed in LSCC tissues, which suggested its tumor suppressor role rather than a tumor facilitator role.…”

Section: Discussionmentioning

confidence: 65%

MiR‐372‐3p promotes cell growth and metastasis by targeting FGF9 in lung squamous cell carcinoma

et al. 2017

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The aim of this study was to study the role of miR‐372‐3p in lung squamous cell carcinoma (LSCC) cell proliferation and invasion by suppressing FGF9. RT‐PCR was used to determine miR‐372‐3p and FGF9 mRNA expression in tissues and cells. Western blot was used to determine FGF9 expression in tissues and NCI‐H520 cell line. Dual luciferase reporter gene assay was conducted to confirm that FGF9 can be directly targeted by miR‐372‐3p. MTT, colony formation assays were conducted to investigate the effects of ectopic miR‐372‐3p and FGF9 expression on NCI‐H520 cell growth. Flow cytometry was used to analyze the influence of miR‐372‐3p and FGF9 expression on cell cycle distribution and apoptosis. Transwell assay was also conducted to see the effects of miR‐372‐3p and FGF9 expression on NCI‐H520 cell invasiveness. MiR‐372‐3p was found significantly overexpressed in both LSCC tissues and cell lines, whereas FGF9 mRNA was found underexpressed in LSCC tissues. MiR‐372‐3p directly bound to wild‐type FGF9 mRNA 3′UTR, therefore led to the reduction in FGF9 expression. The upregulation of FGF9 or the downregulation of miR‐372‐3p substantially retarded LSCC cell growth, mitosis, and invasion. MiR‐372‐3p enhanced LSCC cell proliferation and invasion through inhibiting FGF9.

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Section: Discussionmentioning

confidence: 65%

MiR‐372‐3p promotes cell growth and metastasis by targeting FGF9 in lung squamous cell carcinoma

et al. 2017

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“…Despite previous studies by us and others showing rigid regulations at pre- (22,23) and post-transcriptional levels (24,25), overexpressed FGF9 protein is frequently observed in various cancer cells (17–20). Although aberrant expression of FGF9 is known to promote cancer progression in many cancers including colon cancer (36–38), the mechanism of how FGF9 protein is elevated in cancer cells remains largely unknown. As translational control provides cells with the plasticity and flexibility to respond to rapid changes in the environment, we hypothesized the increase of FGF9 protein resulted from the response to the microenvironmental change (i.e.hypoxia) in the cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of FGF9 in colon cancer cells is mediated by hypoxia-induced translational activation

Chen¹,

Shih²,

Tseng³

et al. 2013

Nucleic Acids Research

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Human fibroblast growth factor 9 (FGF9) is a potent mitogen involved in many physiological processes. Although FGF9 messenger RNA (mRNA) is ubiquitously expressed in embryos, FGF9 protein expression is generally low and restricted to a few adult organs. Aberrant expression of FGF9 usually results in human malignancies including cancers, but the mechanism remains largely unknown. Here, we report that FGF9 protein, but not mRNA, was increased in hypoxia. Two sequence elements, the upstream open reading frame (uORF) and the internal ribosome entry site (IRES), were identified in the 5' UTR of FGF9 mRNA. Functional assays indicated that FGF9 protein synthesis was normally controlled by uORF-mediated translational repression, which kept the protein at a low level, but was upregulated in response to hypoxia through a switch to IRES-dependent translational control. Our data demonstrate that FGF9 IRES functions as a cellular switch to turn FGF9 protein synthesis ‘on’ during hypoxia, a likely mechanism underlying FGF9 overexpression in cancer cells. Finally, we provide evidence to show that hypoxia-induced translational activation promotes FGF9 protein expression in colon cancer cells. Altogether, this dynamic working model may provide a new direction in anti-tumor therapies and cancer intervention.

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“…The proportion of cells stained and the staining intensity score were assessed by the pathologist as follows: 0, absence of staining; 1, weakly stained; 2, moderately stained; and 3, strongly stained. The total score was calculated by multiplying the proportion score with the intensity score [2, 36, 37]. High expression of FGF9 means that the expression of FGF9 is higher than that of normal tissue adjacent to cancer.…”

Section: Methodsmentioning

confidence: 99%

The anti-apoptotic and prognostic value of fibroblast growth factor 9 in gastric cancer

et al. 2016

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Fibroblast growth factor (FGF) 9 is a member of the FGF family, which promotes carcinogenesis in some solid tumours. However, its biological and prognostic significance in gastric cancer (GC) is unclear. We examined FGF9 expression in 180 GC and corresponding non-tumorous gastric tissue samples by immunohistochemistry and evaluated its role in predicting tumour prognosis. Knockdown of FGF9 by siRNA inhibited cell growth and induced apoptosis in GC cell lines. Fifty of the 180 GC specimens (27.8%) had high FGF9 protein expression, whereas decreased or unchanged expression was observed in 130 cases (72.2%). High FGF9 expression was a significant predictor of poor survival (28.1 vs. 55.8 months, P < 0.001). After stratification according to AJCC stage, FGF9 remained a significant predictor of shorter survival in stage II (30.6 vs. 64.9 months, P < 0.001) and stage III GC (29.7 vs. 58.9 months, P < 0.001). Multivariate and univariate analysis showed that higher expression of FGF9 can be used as a predictor for poor prognosis (HR, 2.95; 95% CI, 1.97–4.41; P < 0.001; and HR, 2.94; 95% CI, 2.01–4.31; P < 0.001, respectively). FGF9 may provide the anti-apoptotic function and be useful as a novel independent marker for evaluating GC prognosis

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Relationship between the localization of fibroblast growth factor 9 in prostate cancer cells and postoperative recurrence

Cited by 22 publications

References 25 publications

MiR‐372‐3p promotes cell growth and metastasis by targeting FGF9 in lung squamous cell carcinoma

MiR‐372‐3p promotes cell growth and metastasis by targeting FGF9 in lung squamous cell carcinoma

Overexpression of FGF9 in colon cancer cells is mediated by hypoxia-induced translational activation

The anti-apoptotic and prognostic value of fibroblast growth factor 9 in gastric cancer

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