Silencing of Forkhead box D1 inhibits proliferation and migration in glioma cells

Gao, Yuanfeng; Zhu, Tao; Mao, Xiao‐Yuan; Mao, Chen-Xue; Li, Ling; Yin, Ji‐Ye; Zhou, Hong‐Hao; Liu, Zhao‐Qian

doi:10.3892/or.2017.5344

Cited by 35 publications

(37 citation statements)

References 30 publications

(30 reference statements)

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“…Knockdown of FOXD1 significantly inhibited proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo, and increased the apoptosis rates of NSCLC cells. The results were consistent with other studies, which showed significant growth inhibition in several cancer cell types [7,10,21]. In breast cancer, it was suggested that FOXD1 induces the G1/S transition and promotes the cell cycle progression by down-regulation of p27 expression [10].…”

Section: Discussionsupporting

confidence: 82%

“…In breast cancer, it was suggested that FOXD1 induces the G1/S transition and promotes the cell cycle progression by down-regulation of p27 expression [10]. In glioma, reduced expression of FOXD1 was associated with the inhibition of glioma cell proliferation, cell survival and migration, implying that FOXD1 is an oncogene in glioma [21]. It was found that knockout of FOXD1 inhibits downstream transcriptional Dax1, which is a component of the autoregulatory network for maintaining pluripotency, and the fate mapping analyses further reveal that >95% of induced pluripotent stem cell (iPSC) colonies are derived from FOXD1-positive cells.…”

Section: Discussionmentioning

confidence: 99%

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FOXD1 Promotes Cell Growth and Metastasis by Activation of Vimentin in NSCLC

Fan

et al. 2018

Cell Physiol Biochem

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Background/Aims: Forkhead box D1 (FOXD1) has a well-established role in early embryonic development and organogenesis and functions as an oncogene in several cancers. However, the clinical significance and biological roles of FOXD1 in non-small cell lung cancer (NSCLC) remain largely unknown. Methods: A total of 264 primary NSCLC tissue samples were collected. The expression levels of FOXD1 in these samples were examined by immunohistochemical staining. The expression of FOXD1 was knocked down by lentiviral shRNA. The relative expression of FOXD1 was determined by qRT-PCR, Western blotting and immunofluorescence image. The functional roles of FOXD1 in NSCLC were demonstrated cell viability CCK-8 assay, colony formation, cell invasion and migration assays, and cell apoptosis assay in vitro. In vivo mouse xenograft and metastasis models were used to assess tumorigenicity and metastatic ability. The Chi-square test was used to assess the correlation between FOXD1 expression and the clinicopathological characteristics. Survival curves were estimated by Kaplan-Meier method and compared using the log-rank test. The Cox proportional hazards model was used for univariate and multivariate analyses. Results: We determined that higher levels of FOXD1 were present in NSCLC tissues, especially in metastatic NSCLC tissues. FOXD1 was also higher in all NSCLC cells compared with normal human bronchial epithelial cells. A higher expression level of FOXD1 was associated with malignant behavior and poor prognosis in NSCLC patients. Knockdown of FOXD1 significantly inhibited proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo, and it increased the apoptosis rates of NSCLC cells. Mechanistic analyses revealed that FOXD1 expressed its oncogenic characteristics through activating Vimentin in NSCLC. Multivariate Cox regression analysis indicated that FOXD1 was an independent prognostic factor both for overall survival (OS) and disease-free survival (DFS) in NSCLC patients. Conclusion: Our results indicated that FOXD1 might be involved in the development and progression of NSCLC as an oncogene, and thereby might be a potential therapeutic target for NSCLC patients.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

FOXD1 Promotes Cell Growth and Metastasis by Activation of Vimentin in NSCLC

Fan

et al. 2018

Cell Physiol Biochem

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“…The proposed nomogram demonstrated that the risk score was one of the most important indicators for prognosis. Among the included genes, FOXD1 has previously been reported to promote migration and to be associated with drug resistance in glioma (12). CCNA2 was revealed to correlate closely with distant metastasis-free, recurrence-free and overall survival in breast cancer; in addition, it also contributes to tamoxifen resistance in patients with ER+ breast cancer (13).…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic signature predicts the distant relapse in patients with ER+ breast cancer treated with tamoxifen for five years

Zhou

Guo

2017

Mol Med Report

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Tamoxifen is the most commonly used drug to treat estrogen receptor positive (ER+) breast cancer. However, many patients with ER+ breast cancer have experienced resistance and other adverse side effects following treatment with tamoxifen. Furthermore, clinical and pathological parameters have thus far failed to predict the efficiency of tamoxifen administration. Therefore, gene signature based models for the prediction of survival time of such patients are urgently needed. In the current study, gene expression levels and follow‑up information of samples from GSE17705 and GSE22219 databases were used to construct a risk score model based on Cox multivariate regression. The expression levels of 10 genes were included in the model: CCNB2, CCNA2, FOXD1, WSB2, RBPMS, CTDSP1, BIN3, SLBP, EPRS, FTO. The samples in the high‑risk group had a relative early distant relapse time period (median survival time of 3.75 years) compared with the patients in the low risk group (median survival time of 6.5 years, P<0.01). For further validation, a further two independent datasets (GSE26971, GSE58644) were assessed. The overall survival time period of patients with high‑risk scores in these datasets was significantly longer than those with low‑risk scores (P<0.01). Furthermore, the associations between clinical parameters and risk score were investigated, and it was revealed that the risk score was significantly correlated with tumor age, tumor stage and grade. In addition, a 5‑year survival nomogram was plotted in order to facilitate the utilization of risk score along with other clinical data. In summary, using the transcriptomic profile, a multi‑gene expression based risk score was developed and was revealed as being able to successfully predict the outcome of patients with ER+ breast cancer treated with tamoxifen for 5 years.

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“…Total RNA of glioma cell lines or tissues was isolated with RNAiso Plus (Takara, China) and reverse‐transcribed into cDNA by PrimeScript™ RT reagent Kit (Takara). The PCR amplification procedure using the LightCycler ® 480 Instrument (Roche, Switzerland) was described previously . Briefly, 2 μL cDNA template was amplified in a 20‐μL reaction mix system of SYBR Green (Takara) under the following conditions: 30 s at 95°C, followed by 40 cycles of three reaction steps with different temperatures (5 s at 95°C, 30 s at 55°C, and 30 s at 72°C).…”

Section: Methodsmentioning

confidence: 99%