c-Fos/microRNA-18a feedback loop modulates the tumor growth via HMBOX1 in human gliomas

Zhou, Jingbin; Wang, Muchun; Deng, Dongfeng

doi:10.1016/j.biopha.2018.08.157

Cited by 17 publications

(11 citation statements)

References 38 publications

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“…It is related to the plasticity of neurons and can affect the formation of cell memory by participating in the regulation of neuropeptides (15). In the pathological state, the FOS gene is related to the occurrence and development of a variety of malignant tumors (16)(17)(18) such as ovarian cancer (19), as well as brain diseases (20,21). In this study, the high expression of FOS in ESCA was confirmed by bioinformatics methods, and the above conclusion was further verified by IHC.…”

Section: Discussionsupporting

confidence: 63%

Screening and verification of potential gene targets in esophageal carcinoma by bioinformatics analysis and immunohistochemistry

Wen¹,

Dayyani²,

Tao³

et al. 2022

Ann Transl Med

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Background: To evaluate the potential of candidate proteins as diagnostic markers or drug targets in esophageal carcinoma (ESCA).Methods: GSE20347, GSE17351, and GSE45670 were downloaded from Gene Expression Omnibus (GEO). Differently expressed genes (DEGs) between ESCA and normal esophageal tissues from patients were obtained. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed. The genes commonly featured in ESCA were screened by least absolute shrinkage and selection operator (LASSO) logistic regression and Boruta feature selection algorithm. The transcriptome data and corresponding clinical data of ESCA were downloaded from The Cancer Genome Atlas (TCGA) public database. Kaplan-Meier survival analysis was used to explore the core genes related to the prognosis of patients. A protein-protein interaction (PPI) network was generated by GeneMANIA to visualize the functional network between genes. Expressions of CRIP2, FOS, and HOXA10 genes in ESCA cells were verified by immunohistochemistry (IHC).Results: Out of 11,207 genes, 430 DEGs were identified, including 210 up-regulated genes and 220 downregulated genes. After taking the intersection of LASSO regression and Boruta algorithm, 15 core genes were identified. Survival analyses demonstrated that low expression of CRIP2 (P=2.643e-02), as well as high expression of FOS (P=4.837e-02) and HOXA10 (P=4.97e-02), was significantly associated with the worse prognosis of ESCA patients. The 3 genes were strongly correlated with the content of immune cells and the stage of tumors. The expression of CRIP2 was correlated with the sensitivity of patients to dasatinib; FOS expression was correlated with the sensitivity of patients to erlotinib, and HOXA10 expression affected the sensitivity of patients to cisplatin, dasatinib, erlotinib, and gefitinib. The cBioportal database showed that 56 patients (31%) had the above core gene mutations: CRIP2 (8%), FOS (10%), and HOXA10 (17%). The IHC showed that there were differences in the expressions of these core genes between ESCA patients and the normal population (P<0.05), with ESCA patients showing higher expression. Conclusions:The low CRIP2 expression and high expressions of FOS and HOXA10 are associated with more advanced tumor stage, which may have the potential to be novel biomarkers for treatment selection in ESCA.

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Section: Discussionsupporting

confidence: 63%

Screening and verification of potential gene targets in esophageal carcinoma by bioinformatics analysis and immunohistochemistry

Wen¹,

Dayyani²,

Tao³

et al. 2022

Ann Transl Med

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“…A previous study showed that HMBOX1 expression in HGSOC tissues and ovarian cancer cell lines was significantly lower than that in ovarian epithelial tissues or normal ovarian epithelial cell lines, and overexpression of HMBOX1 suppressed proliferation of the A2780 cell line 31. In human gliomas, the c-Fos/miR-18a feedback loop increased tumor growth via HMBOX1 32. In liver cancer, HMBOX1 inhibited tumor progression via elevating the autophagy level as well as suppressing stemness and immune escape 33.…”

Section: Discussionmentioning

confidence: 99%

<p>tRNA-derived fragment tRF-03357 promotes cell proliferation, migration and invasion in high-grade serous ovarian cancer</p>

Zhang

Wang

et al. 2019

OTT

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Background High-grade serous ovarian cancer (HGSOC) is one of the most common ovarian epithelial malignancies. tRNA-derived fragments (tRFs) have been identified as novel potential biomarkers and targets for cancer therapy. Nevertheless, the influence of tRFs on HGSOC remains unknown. This study aimed to identify HGSOC-associated tRFs and to investigate the function and mechanism of key tRFs in SK-OV-3 ovarian cancer cells. Methods The tRF profiles in HGSOC patients and controls were investigated using small RNA sequencing. Differentially expressed tRFs were verified by real-time PCR, and a key tRF was evaluated in a function study. Results A total of 27 tRFs were differentially expressed between HGSOC patients and controls. Differentially expressed tRFs were mainly involved in the functions of protein phosphorylation, transcription and cell migration and the pathway of cancer, and the MAPK and Wnt signaling pathways. Real-time PCR verified that tRF-03357 and tRF-03358 were significantly increased in the HGSOC serum samples and SK-OV-3 cells compared to their expression levels in the controls. Importantly, tRF-03357 promoted SK-OV-3 cell proliferation, migration and invasion. Moreover, tRF-03357 was predictively targeted, and significantly downregulated HMBOX1. Conclusion This study suggests that tRF-03357 might promote cell proliferation, migration and invasion, partly by modulating HMBOX1 in HGSOC.

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“…With the aim of downregulating this inhibitor, the intensification via transfection of miR-18a, of the miR-17 to miR-92 cluster, might hamper the chaotic and unfettered growth of BAVMs, even following subtotal surgical resection or embolization. Although miR-17, miR-18a, miR-19a, and miR-20a have displayed antiangiogenic and tumor suppressive activity, most notably when considered independently, they have also been connected to oncogenesis and neoplastic angiogenesis [17,54,55]. The majority of members belonging to the miR-17-92 cluster were upregulated in pediatric brain tumors including medulloblastomas, ependymomas, and astrocytomas, with the highest expression being noticed for miR-18a and miR-18b [56].…”

Section: Mir-18amentioning

confidence: 99%

An Insight into the microRNAs Associated with Arteriovenous and Cavernous Malformations of the Brain

Florian

Buruiană

Şuşman

et al. 2021

Cells

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Background: Brain arteriovenous malformations (BAVMs) and cerebral cavernous malformations (CCMs) are rare developmental anomalies of the intracranial vasculature, with an irregular tendency to rupture, and as of yet incompletely deciphered pathophysiology. Because of their variety in location, morphology, and size, as well as unpredictable natural history, they represent a management challenge. MicroRNAs (miRNAs) are strands of non-coding RNA of around 20 nucleotides that are able to modulate the expression of target genes by binding completely or partially to their respective complementary sequences. Recent breakthroughs have been made on elucidating their contribution to BAVM and CCM occurrence, growth, and evolution; however, there are still countless gaps in our understanding of the mechanisms involved. Methods: We have searched the Medline (PubMed; PubMed Central) database for pertinent articles on miRNAs and their putative implications in BAVMs and CCMs. To this purpose, we employed various permutations of the terms and idioms: ‘arteriovenous malformation’, ‘AVM’, and ‘BAVM’, or ‘cavernous malformation’, ‘cavernoma’, and ‘cavernous angioma’ on the one hand; and ‘microRNA’, ‘miRNA’, and ‘miR’ on the other. Using cross-reference search; we then investigated additional articles concerning the individual miRNAs identified in other cerebral diseases. Results: Seven miRNAs were discovered to play a role in BAVMs, three of which were downregulated (miR-18a, miR-137, and miR-195*) and four upregulated (miR-7-5p, miR-199a-5p, miR-200b-3p, and let-7b-3p). Similarly, eight miRNAs were identified in CCM in humans and experimental animal models, two being upregulated (miR-27a and mmu-miR-3472a), and six downregulated (miR-125a, miR-361-5p, miR-370-3p, miR-181a-2-3p, miR-95-3p, and let-7b-3p). Conclusions: The following literature review endeavored to address the recent discoveries related to the various implications of miRNAs in the formation and growth of BAVMs and CCMs. Additionally, by presenting other cerebral pathologies correlated with these miRNAs, it aimed to emphasize the potential directions of upcoming research and biological therapies.

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c-Fos/microRNA-18a feedback loop modulates the tumor growth via HMBOX1 in human gliomas

Cited by 17 publications

References 38 publications

Screening and verification of potential gene targets in esophageal carcinoma by bioinformatics analysis and immunohistochemistry

Screening and verification of potential gene targets in esophageal carcinoma by bioinformatics analysis and immunohistochemistry

<p>tRNA-derived fragment tRF-03357 promotes cell proliferation, migration and invasion in high-grade serous ovarian cancer</p>

An Insight into the microRNAs Associated with Arteriovenous and Cavernous Malformations of the Brain

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