Fibroblast growth factor�18 promotes the growth, migration and invasion of MDA‑MB‑231 cells

Yu, Ziyi; Lou, Longquan; Zhao, Yi

doi:10.3892/or.2018.6482

Cited by 13 publications

(14 citation statements)

References 38 publications

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“…3 a). Previous studies suggested that the amplification of FGF18 was found in a number of solid tumors, and its overexpression was significantly correlated with poor prognosis [ 21 – 24 ]. Considering the important roles of both FGF18 and HDAC7 in NSCLC progression, we were interested in investigating their regulatory relationship and underlying mechanisms.…”

Section: Resultsmentioning

confidence: 99%

“…In the present study, we focused on FGF18, which is involved in HDAC7-mediated NSCLC progression. Previous studies have reported a prominent role of FGF18 in tumorigenesis, proliferation, and metastasis of several tumors, including gastric cancer, ovarian cancer, and breast cancer [ 21 , 22 , 24 ]. Chen et al found that the FGF18 could promote proliferation and migration of large cell lung carcinoma (LCLC) cells [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

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HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway

Guo

Zhang

et al. 2022

J Exp Clin Cancer Res

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Background Histone deacetylases (HDACs) play crucial roles in cancers, but the role and mechanism of HDAC7 in NSCLC have not been fully understood. Methods A total of 319 patients with non-small cell lung cancer (NSCLC) who underwent surgery were enrolled in this study. Immunohistochemistry and Kaplan–Meier survival analysis were performed to investigate the relationship between HDAC7, fibroblast growth factor 18 (FGF18) expression, and clinicopathologic characteristics. Cell functional experiments were implemented both in vivo and in vitro to investigate the effects on NSCLC cell proliferation and metastasis. Recombinant lentivirus–meditated in vivo gene overexpression or knockdown, real-time polymerase chain reaction (PCR), western blotting, and coimmunoprecipitation assays were applied to clarify the underlying molecular mechanism of HDAC7 in promoting NSCLC progression. Results The elevated expression of HDAC7 or FGF18 was positively correlated with poor prognosis, tumor–node–metastasis (TNM) stage, and tumor differentiation of NSCLC patients. NSCLC patients with co-expressed HDAC7 and FGF18 suffered the worst prognosis. HDAC7 overexpression promoted NSCLC proliferation and metastasis by upregulating FGF18. Conversely, overexpression of FGF18 reversed the attenuated ability in tumor growth and metastasis mediated by downregulating HDAC7. In terms of mechanism, our results suggested that the interaction of HDAC7 with β-catenin caused decreased β-catenin acetylation level at Lys49 and decreased phosphorylation level at Ser45. As a consequence, the HDAC7-mediated posttranslational modification of β-catenin facilitated nuclear transfer and activated FGF18 expression via binding to TCF4. Furthermore, deubiquitinase USP10 interacted with and stabilized HDAC7. The suppression of USP10 significantly accelerated the degradation of HDAC7 and weakened NSCLC growth and migration. Conclusions Our findings reveal that HDAC7 promotes NSCLC progression through being stabilized by USP10 and activating the β-catenin-FGF18 pathway. Targeting this novel pathway may be a promising strategy for further developments in NSCLC therapy.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway

Guo

Zhang

et al. 2022

J Exp Clin Cancer Res

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“…Conversely, different from human breast cancer, miR-21 had a very high likelihood of targeting to 3′ UTR of the fibroblast growth factor 18 FGF18 (score 97 in miRDB) mRNA. In breast cancer, FGF18 promotes cell proliferation through the ERK/c-Myc signaling pathway and stimulates the production of epithelial-to-mesenchymal transition (EMT) factors, thus, promoting neoplastic cell migration and invasion [ 47 ]. Noteworthy, in the current study, the highest level of miR-21 expression was observed in the two malignant tumors with evidence of neoplastic emboli in lymphatic vessels (i.e., tubular carcinoma, grade III; inflammatory carcinoma, grade III) (Data not shown).…”

Section: Discussionmentioning

confidence: 99%

RT-qPCR Expression Profiles of Selected Oncogenic and Oncosuppressor miRNAs in Formalin-Fixed, Paraffin-Embedded Canine Mammary Tumors

Abbate

Giannetto

Arfuso

et al. 2022

Animals

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MicroRNAs (miRNAs) can act as oncogenes or oncosuppressor genes, and their involvement in nearly all cancer-associated processes makes these small molecules promising diagnostic and prognostic biomarkers in cancer, as well as specific targets for cancer therapy. This study aimed to investigate the expression of 7 miRNAs (miR-18a, miR-18b, miR-22, miR-124, miR-145, miR-21, miR-146b) in formalin-fixed, paraffin-embedded canine mammary tumors (CMTs) by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Twenty-six mammary samples were selected, including 22 CMTs (7 benign; 15 malignant) and 4 control samples (3 normal mammary gland and 1 case of lobular hyperplasia). Oncogenic miR-18a, miR-18b and miR-21 were significantly upregulated in malignant tumors compared with control tissues (p < 0.05). Conversely, oncosuppressor miR-146b was significantly downregulated in benign and malignant mammary tumors compared with control samples (p < 0.05) while, no group-related differences in the expression levels of miR-22, miR-124 and miR-145 were found (p > 0.05). Upregulated miRNAs found here, may regulate genes involved in receptor-mediated carcinogenesis and proteoglycan remodeling in cancer; while miRNA with reduced expression can regulate genes involved in Toll-like receptor and MAPK signaling pathways. According to the results obtained in the current study, the oncogenic and oncosuppressor miRNAs analyzed here are dysregulated in CMTs and the dysregulation of miRNA targets may lead to specific altered cellular processes and key pathways involved in carcinogenesis. Of note, since oncogenic miRNAs predicted to regulate neoplastic cell proliferation and hormonal activities, they may play an active role in neoplastic transformation and/or progression, having mechanistic and prognostic relevance in CMTs.

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“…FGF8 signalling increases oestrogen-induced breast cancer cell proliferation by inducing the expression of the ER mRNA, and at the same time suppresses the inhibition of mitosis by activating the cell cycle regulator CDC2 and other regulators of cell cycle entry [ 164 , 165 ]. The increased expression of FGF18 mRNA and protein has been associated with migration in vitro and poor overall survival in cancer patients [ 166 ]. A recent study showed that FGF18 increased cell migration and EMT through AKT signalling and by inducing the transcription of proliferation-related genes, including CDC2 , metastasis-related genes ( TGFβ , MMP-2 and MMP-9 ) and EMT markers like the SNAIL proteins and N -cadherin [ 167 ].…”

Section: Fgfs In Breast Cancermentioning

confidence: 99%

Fibroblast growth factor receptor signalling dysregulation and targeting in breast cancer

Francavilla

O'Brien

2022

Open Biol.

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Fibroblast Growth Factor Receptor (FGFR) signalling plays a critical role in breast embryonal development, tissue homeostasis, tumorigenesis and metastasis. FGFR, its numerous FGF ligands and signalling partners are often dysregulated in breast cancer progression and are one of the causes of resistance to treatment in breast cancer. Furthermore, FGFR signalling on epithelial cells is affected by signals from the breast microenvironment, therefore increasing the possibility of breast developmental abnormalities or cancer progression. Increasing our understanding of the multi-layered roles of the complex family of FGFRs, their ligands FGFs and their regulatory partners may offer novel treatment strategies for breast cancer patients, as a single agent or rational co-target, which will be explored in depth in this review.

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Fibroblast growth factor�18 promotes the growth, migration and invasion of MDA‑MB‑231 cells

Cited by 13 publications

References 38 publications

HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway

HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway

RT-qPCR Expression Profiles of Selected Oncogenic and Oncosuppressor miRNAs in Formalin-Fixed, Paraffin-Embedded Canine Mammary Tumors

Fibroblast growth factor receptor signalling dysregulation and targeting in breast cancer

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