Expression and potential role of FOSB in glioma

Qi, Min; Sun, Lean; Zheng, Lan-rong; Zhang, Jia; Han, Yanling; Wu, Feng; Zhao, Jun; Niu, Wenhao; Fei, Mao-xing; Jiang, Xiaochun; Zhou, Meng-Liang

doi:10.3389/fnmol.2022.972615

Cited by 3 publications

(2 citation statements)

References 35 publications

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“…When FOSB is downregulated, glioma cell viability decreases, and the proliferation and migration ability of glioma cells decreases. This may promote the development and migration of glioma cells and decrease the survival of non-small cell lung cancer (NSCLC) patients [14,15] . There are also studies showing that FOSB is associated with in ammation after myocardial cell infarction [16] .…”

Section: Discussionmentioning

confidence: 99%

The role of S100A9 in the progression of tuberculosis

Liu,

Duan,

Tong

et al. 2024

Preprint

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Objective: Elevated plasma levels of S100A9 have been observed in patients with severe tuberculosis, with further increases in patients with poor prognosis, suggesting that S100A9 is a potential biomarker for disease progression and prognosis. However, the molecular mechanism underlying its potential remains unclear, highlighting the importance of exploring its function. Methods: To further investigate the role of S100A9 in severe tuberculosis, we constructed S100A9 gene knockout or overexpression models and analyzed the transcriptome changes in THP-1 cells following S100A9 overexpression or shRNA silencing using next-generation sequencing. Through the analysis of transcriptome sequencing results, we identified eight genes that may be involved in the regulation of S100A9 expression. We also detected the expression of the S100A9 gene and related differentially expressed genes after Mycobacterium tuberculosisinfection, as well as their enrichment and related pathways. It was inferred that S100A9 may be involved in the mechanism by which tuberculosis progresses to severe tuberculosis. Results: FOSB and IL17c are potentially related to the IL-17 signaling pathway, while calcium/calmodulin-dependent protein kinase II beta (CAMK2B) may be related to the ErbB signaling pathway. These findings indicate that these genes may promote the progression of tuberculosis through different mechanisms. Conclusion: Our study explored the potential role and mechanism of S100A9 in the development of tuberculosis, providing a new perspective for the development of treatment strategies for this disease.

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Section: Discussionmentioning

confidence: 99%

The role of S100A9 in the progression of tuberculosis

Liu,

Duan,

Tong

et al. 2024

Preprint

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“…The FOS gene encodes a transcription factor that co-localise with members of the Jun family, including c-Jun, JunB and JunD, and regulate cell proliferation, tumor invasion, distant metastasis and angiogenesis ( 50 ). FOSB is upregulated in tumors and knockdown of FOSB decreases migration ability ( 51 ). ZFP36 inhibits prostate cancer progression by targeting CDK6 and oxidative stress ( 52 ).…”

Section: Discussionmentioning

confidence: 99%

Early growth response 1 regulates dual‑specificity protein phosphatase 1 and inhibits cell migration and invasion of tongue squamous cell carcinoma

Zhou,

Shan,

et al. 2024

Oncol Lett

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Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors in the head and neck, and among the OSCCs, tongue squamous cell carcinoma (TSCC) is one of the most common types. Although therapy strategies have recently advanced, the prognosis of TSCC has not substantially improved. Metastasis is one of the main causes of patient mortality in TSCC; therefore, it is necessary to elucidate the mechanism by which TSCC metastasis is regulated. In the present study, the early growth response 1 (Egr-1) expression in TSCC was analyzed based on GEO datasets and the effect of Egr-1 in TSCC tumor cell migration and invasion was measured using Transwell assay. By overexpressing dual-specificity protein phosphatase 1 (DUSP1) in cells with Egr-1 knockdown using lentivirus infection, the role of DUSP1 in Egr-1-regulated TSCC cell migration and invasion was determined. By using luciferase and ChIP assays, the mechanism behind how DUSP1 is regulated by Egr-1 was detected. In the present study, it was demonstrated that Egr-1 was downregulated in TSCC and the knockdown of Egr-1 increased TSCC cell migration and invasion. The expression of Egr-1 was also correlated with DUSP1. The overexpression of DUSP1 in Egr-1 knockdown cells, reduced the level of cell migration and invasion. Furthermore, it was demonstrated that knockdown of Egr-1 inhibited the promoter activity of DUSP1 and the site through which Egr-1 regulates DUSP1 transcription was identified. In conclusion, the present study demonstrated that Egr-1 regulates TSCC cell migration and invasion through modulating DUSP1, suggesting the potential of Egr-1 and DUSP1 as therapy targets for TSCC.

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In vivo loss of tumorigenicity in a patient-derived orthotopic xenograft mouse model of ependymoma

et al. 2023

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IntroductionEpendymomas (EPN) are the third most common malignant brain cancer in children. Treatment strategies for pediatric EPN have remained unchanged over recent decades, with 10-year survival rates stagnating at just 67% for children aged 0-14 years. Moreover, a proportion of patients who survive treatment often suffer long-term neurological side effects as a result of therapy. It is evident that there is a need for safer, more effective treatments for pediatric EPN patients. There are ten distinct subgroups of EPN, each with their own molecular and prognostic features. To identify and facilitate the testing of new treatments for EPN, in vivo laboratory models representative of the diverse molecular subtypes are required. Here, we describe the establishment of a patient-derived orthotopic xenograft (PDOX) model of posterior fossa A (PFA) EPN, derived from a metastatic cranial lesion.MethodsPatient and PDOX tumors were analyzed using immunohistochemistry, DNA methylation profiling, whole genome sequencing (WGS) and RNA sequencing.ResultsBoth patient and PDOX tumors classified as PFA EPN by methylation profiling, and shared similar histological features consistent with this molecular subgroup. RNA sequencing revealed that gene expression patterns were maintained across the primary and metastatic tumors, as well as the PDOX. Copy number profiling revealed gains of chromosomes 7, 8 and 19, and loss of chromosomes 2q and 6q in the PDOX and matched patient tumor. No clinically significant single nucleotide variants were identified, consistent with the low mutation rates observed in PFA EPN. Overexpression of EZHIP RNA and protein, a common feature of PFA EPN, was also observed. Despite the aggressive nature of the tumor in the patient, this PDOX was unable to be maintained past two passages in vivo.DiscussionOthers who have successfully developed PDOX models report some of the lowest success rates for EPN compared to other pediatric brain cancer types attempted, with loss of tumorigenicity not uncommon, highlighting the challenges of propagating these tumors in the laboratory. Here, we discuss our collective experiences with PFA EPN PDOX model generation and propose potential approaches to improve future success in establishing preclinical EPN models.

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Expression and potential role of FOSB in glioma

Cited by 3 publications

References 35 publications

The role of S100A9 in the progression of tuberculosis

The role of S100A9 in the progression of tuberculosis

Early growth response 1 regulates dual‑specificity protein phosphatase 1 and inhibits cell migration and invasion of tongue squamous cell carcinoma

In vivo loss of tumorigenicity in a patient-derived orthotopic xenograft mouse model of ependymoma

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