Browsing by Subject "EIF4A3"

Now showing 1 - 5 of 5
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    CBP-mediated FOXO4 acetylation facilitates postmenopausal osteoporosis (PMO) progression through the inhibition of the Wnt/β-catenin signaling pathway
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Huang, Qiubo; Wang, Jiang
    FOXO4 was previously identified as a potential biomarker and therapeutic target for postmenopausal osteoporosis (PMO) using bioinformatic analysis, but its specific function and molecular mechanism in the progression of osteoporosis was not reported. The current study was designed to investigate the biological function and underlying mechanism of FOXO4 in PMO. Our results showed that FOXO4 expression was significantly upregulated in the serum samples of PMO patients, which was also negatively correlated with the expression of osteogenesis genes (OCN and ALP). In addition, FOXO4 depletion alleviated osteoporosis by facilitating osteogenic differentiation and inhibiting adipogenic differentiation in human bone marrow mesenchymal stem cells (hBMSCs). Overexpression of FOXO4 exerted the opposite effects on the osteogenic/adipogenic differentiation in hBMSCs. Moreover, FOXO4 knockdown activated the Wnt/β-catenin signaling whereas the inhibition of Wnt/β-catenin signaling overturned the effects of FOXO4 deficiency on osteoporosis. Furthermore, FOXO4 upregulation in PMO was caused by CBP-induced acetylation. In summary, our data demonstrated that FOXO4 was a potent biomarker for PMO and mediated the balance between osteogenesis and adipogenesis in hBMSCs by regulating Wnt/β-catenin signaling
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    CircTADA2A Up-regulates MAPK8 by targeting MiR-214-3p and recruiting EIF4A3 to promote the invasion and migration of non-small cell lung cancer cells
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Zhang, Xi; Lei, Guangyan; Zhao, Kun; Zhang, Xinwei; Dang, Chengxue
    Background. Non-small cell lung cancer (NSCLC) occupies 87% of all lung cancer cases. Due to delayed diagnosis, the prognosis of NSCLC is unfavorable. To improve the survival of patients with NSCLC, more effective therapeutic targets urgently need to be identified. Recently, circular RNAs (circRNAs) have been revealed to play a crucial role in NSCLC progression. Purpose. This research focused on the influence of circTADA2A on the malignant phenotype of NSCLC cells and its in-depth regulatory mechanisms. Methods. RT-qPCR and western blot assays were done to examine the level of gene/protein of interest. Wound healing and transwell assays were conducted to monitor the migration and invasion of NSCLC cells. Bioinformatics tools and mechanistic assays were utilized to delve into the underlying mechanism of circTADA2A in NSCLC cells. Results. The results demonstrated that circTADA2A presented a high expression in NSCLC. CircTADA2A knockdown was revealed to hamper migration and invasion of NSCLC cells. Mechanistically, circTADA2A elevated MAPK8 expression through sequestering miR214-3p and recruiting EIF4A3. Conclusion. CircTADA2A enhances MAPK8 expression by serving as a miR-214-3p sponge and EIF4A3 decoy, consequently promoting invasion and migration of NSCLC cells.
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    Extra-meningeal solitary fibrous tumor: an evolving entity with chameleonic morphological diversity, a hallmark molecular alteration and unresolved issues in risk stratification assessment
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Machado, Isidro; Giner, Francisco; Cruz, Julia; Lavernia, Javier; Marhuenda Fluixa, Ana; Claramunt, Reyes; López Guerrero, José Antonio; Navarro, Samuel; Ferrandez, Antonio; Blázquez Bujeda, Álvaro; Ruiz-Sauri, Amparo; Llombart Bosch, Antonio
    Solitary fibrous tumor (SFT) is a rare type of mesenchymal lesion with variable clinical presentation in which specific clinicopathologic factors have been related to patient outcome. SFT shares an important morphologic and immunohistochemical overlap with other sarcomas, hence the differential diagnosis is challenging. Although molecular studies provide significant clues, especially in the differential diagnosis with other neoplasms, a thorough hematoxylin and eosin analysis and the integration of phenotypical, clinical, and radiological features remain an essential tool in SFT diagnosis. In this review, we discuss some emerging issues still under debate in SFT.
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    Knockdown of circular RNA hsa_circ_0062270 suppresses the progression of melanoma via downregulation of CDC45
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Hao, Tian; Yang, Yi; He, Juan; Bai, Jia; Zheng, Yongjian; Luo, Zhanpeng
    Background. Although systemic therapies for melanoma have been improved, the 5-year survival rate of this aggressive cancer remains poor. It has been shown that hsa_circ_0062270 was upregulated in patients with melanoma. However, the relevant mechanism of hsa_circ_0062270 in the progression of melanoma remains unclear. Methods. The CCK-8, EdU staining, flow cytometry, and transwell assays were used to determine the viability, proliferation, apoptosis and invasion in melanoma cells. An in vivo animal study was performed finally. Results. The level of hsa_circ_0062270 was significantly upregulated in melanoma cells. In addition, hsa_circ_0062270 knockdown markedly inhibited the viability, proliferation, invasion and promoted the apoptosis of melanoma cells. Cell division cycle protein 45 (CDC45) is the host gene of hsa_circ_0062270, and downregulation of hsa_circ_0062270 notably decreased the expression of CDC45 in melanoma cells. Rescue assays confirmed that hsa_circ_0062270 regulated the growth of melanoma cells through CDC45. Moreover, immunoprecipitation (RIP) analysis showed that hsa_circ_0062270 interacted with RNA-binding protein (RBP) EIF4A3. Furthermore, in vivo study indicated that knockdown of hsa_circ_0062270 inhibited the melanoma tumor growth in vivo. Conclusions. Downregulation of hsa_circ_0062270 can inhibit the progression of melanoma through downregulation of CDC45. Our findings provide biological mechanisms for the use of hsa_circ_0062270 as a biomarker for melanoma and potential therapeutic target.
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    Prognostic value of long noncoding RNA LINC00924 in lung adenocarcinoma and its regulatory effect on tumor progression
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Zhang, Wenlong; Zhao, Yanan; Jia, Yuanyuan; Bai, Yuansong
    Purpose. Long non-coding RNAs (lncRNAs) have been used in the study of tumor biomarkers in recent years. However, the prognostic role of lncRNA LINC00924 (LINC00924) in lung adenocarcinoma (LUAD) has not yet been concluded. Therefore, this study investigates the prognostic value of LINC00924 in LUAD and its regulatory effect on tumor progression. Patients and methods. The LUAD tissues and adjacent normal tissues of 128 subjects were extracted, and the expressions of LINC00924 and miR-196a-5p in tissues and cells were detected by RT-qPCR. The prognostic value of LINC00924 in LUAD patients was obtained by Kaplan-Meier analysis and multivariate Cox regression test. The cell counting kit-8 (CCK-8) and Transwell assay were used to detect the effect of overexpression LINC00924 on LUAD cells. Results. In LUAD tissues and cells, LINC00924 expression was down-regulated and miR-196a-5p expression was up-regulated compared with the normal control group. High expression of LINC00924 inhibited the proliferation level, migration ability and invasion situation of LUAD cells, which was more conducive to the survival and prognosis of LUAD patients. Bioinformatics studies indicated that overexpression of LINC00924 inhibited the development of LUAD by targeting miR-196a-5p, while miR-196a-5p mimic effectively weakened the inhibition.Conclusion. LINC00924 sponges of miR-196a-5p may be considered as a potential prognostic biomarker for LUAD.