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FGF5 promotes osteosarcoma cells proliferation via activating MAPK signaling pathway.

ABSTRACT: Objective: This study aimed to investigate the role of fibroblast growth factor-5 (FGF5) in osteosarcoma (OS) and explore the potential mechanisms. Methods: OS gene expression data was downloaded from the Gene Expression Omnibus (GEO; GSE12865) and analyzed by R software. OS tissues and cell lines were collected. The expression level of FGF5 in tumor tissues and cell lines was detected using qRT-PCR. Knockout of FGF5 was performed using CRISPR/Cas9 system. The effects of FGF5 knockout on OS cell proliferation and tumor growth were determined through cell counting kit-8 assay and xenograft nude mice, respectively. Additionally, recombinant FGF5 (rFGF5) was added into OS cell and the effects of rFGF5 on the proliferation and apoptosis of OS cell lines were assayed. Furthermore, the protein expression levels of mitogen-activated protein kinase (MAPK) signaling pathway were detected through Western blot. Results: FGF5 was significantly upregulated in OS tissues and cells, and closely associated with poor differentiation, larger tumor size, lymph node metastasis, and advanced TNM stage. FGF5 knockout could inhibit proliferation of OS cells and tumor growth in nude mouse model. Addition of exogenous rFGF5 promoted OS cell proliferation while inhibited OS cell apoptosis. The expression levels of MAPK signaling pathway proteins in FGF5 knockout group were significantly lower than that in control when there was no rFGF5. Additionally, their expression level in rFGF5 addition group was higher than that in without rFGF5 group. Conclusion: We demonstrated for the first time that FGF5 was overexpressed in OS cell lines and clinical tissue samples and promotes OS cell proliferation by activating MAPK signaling pathway, which indicated that FGF5 was a potential therapeutic target for OS.

SUBMITTER: Han D

PROVIDER: S-EPMC6628182 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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FGF5 promotes osteosarcoma cells proliferation via activating MAPK signaling pathway.

Han Dunxin D Wang Mingming M Yu Zhongkai Z Yin Long L Liu Changli C Wang Jianmin J Liu Yongjun Y Jiang Shengyang S Ren Zhongwu Z Yin Jun J

Cancer management and research 20190710

<b>Objective:</b> This study aimed to investigate the role of fibroblast growth factor-5 (FGF5) in osteosarcoma (OS) and explore the potential mechanisms. <b>Methods:</b> OS gene expression data was downloaded from the Gene Expression Omnibus (GEO; GSE12865) and analyzed by R software. OS tissues and cell lines were collected. The expression level of FGF5 in tumor tissues and cell lines was detected using qRT-PCR. Knockout of FGF5 was performed using CRISPR/Cas9 system. The effects of FGF5 knock ...[more]

PMID: 31372048

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Project description:BackgroundThe deubiquitinating (DUB) enzyme ubiquitin-specific protease 18 (USP18), also known as UBP43, is an ubiquitin-specific protease linked to several human malignancies. However, USP18's underlying function in human cervical cancer remains unclear. In the current study, we aimed to analyse the role of USP18 and its signalling pathways in cervical cancer.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical staining were performed to analyse USP18 levels in cervical cancer and matched to adjacent normal tissues. Moreover, RNA interference (RNAi) and lentiviral-mediated vector transfections were performed to silence and overexpress USP18, respectively, in cervical cancer cells. Further, Cell Counting Kit-8 (CCK-8) and Annexin V/PI staining assays were used to assess its biological function in cell proliferation and apoptosis, respectively. A xenograft model was used to examine USP18's function in vivo.ResultsThe present findings demonstrated that USP18 was overexpressed in cervical cancer specimens and cell lines. Silencing USP18 in SiHa and Caski cervical cancer cell lines inhibited cell proliferation, induced apoptosis, and promoted cleaved caspase-3 expression. In contrast, USP18 overexpression showed the opposite effects in human HcerEpic cells. A Gene Set Enrichment Analysis revealed that USP18 was enriched in the PI3K/AKT signalling pathway in cervical cancer. Hence, the PI3K/AKT inhibitor LY294002 was used to determine the relationship between USP18 and AKT in cervical cancer cells. Importantly, LY294002 significantly abolished the effects of USP18 overexpression in cervical cancer cells. In vivo, USP18 silencing inhibited human cervical cancer cells' tumorigenicity.ConclusionsThe current study indicates that USP18 is an oncogenic gene in cervical cancer. Our findings not only deepened the understanding of USP18's biological function in cervical cancer pathogenesis, but we also provided novel insight for cervical cancer therapy.Trial registrationRetrospectively registered.

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FGF5 promotes osteosarcoma cells proliferation via activating MAPK signaling pathway.

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FGF5 promotes osteosarcoma cells proliferation via activating MAPK signaling pathway.

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