MiR-33a targets FOSL1 and EN2 as a clinical prognostic marker for sarcopenia by glioma

Wang, Wei; Liu, Wei; Xu, Jing; Jin, Hongze

doi:10.3389/fgene.2022.953580

Cited by 4 publications

(4 citation statements)

References 75 publications

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“…Increased copy number and mRNA overexpression of FOSL1 gene are frequently observed in primary breast cancers, independently and irrespectively of the patients’ lymph node axillary metastatic status [ 55 ]. Analysis from transcriptomic FPKM expression data obtained from UCSC Xeba website ( https://xenabrower.net/ ) by Jin’s group demonstrated that FOSL1 can better predict glioma prognosis [ 56 ]. Our previous bioinformatic analysis from TCGA mRNA data showed that FOSL1 serves as a diagnostic and prognostic marker for glioma patients [ 6 ].…”

Section: Discussionmentioning

confidence: 99%

TRPM7 transactivates the FOSL1 gene through STAT3 and enhances glioma stemness

Guo,

Ramar,

Guo

et al. 2023

Cell. Mol. Life Sci.

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Introduction We previously reported that TRPM7 regulates glioma cells’ stemness through STAT3. In addition, we demonstrated that FOSL1 is a response gene for TRPM7, and the FOSL1 gene serves as an oncogene to promote glioma proliferation and invasion. Methods In the present study, we determined the effects of FOSL1 on glioma stem cell (GSC) markers CD133 and ALDH1 by flow cytometry, and the maintenance of stem cell activity by extreme limiting dilution assays (ELDA). To further gain insight into the mechanism by which TRPM7 activates transcription of the FOSL1 gene to contribute to glioma stemness, we constructed a FOSL1 promoter and its GAS mutants followed by luciferase reporter assays and ChIP-qPCR in a glioma cell line and glioma patient-derived xenoline. We further examined GSC markers ALDH1 and TRPM7 as well as FOSL1 by immunohistochemistry staining (IHC) in brain tissue microarray (TMA) of glioma patients. Results We revealed that FOSL1 knockdown reduces the expression of GSC markers CD133 and ALDH1, and FOSL1 is required to maintain stem cell activity in glioma cells. The experiments also showed that mutations of − 328 to − 336 and − 378 to − 386 GAS elements markedly reduced FOSL1 promoter activity. Constitutively active STAT3 increased while dominant-negative STAT3 decreased FOSL1 promoter activity. Furthermore, overexpression of TRPM7 enhanced while silencing of TRPM7 reduced FOSL1 promoter activity. ChIP-qPCR assays revealed that STAT3, present in nuclear lysates of glioma cells stimulated by constitutively activated STAT3, can bind to two GAS elements, respectively. We demonstrated that deacetylation of FOSL1 at the Lys-116 residue located within its DNA binding domain led to an increase in FOSL1 transcriptional activity. We found that the expression of TRPM7, ALDH1, and FOSL1 protein is associated with grades of malignant glioma, and TRPM7 protein expression correlates to the expression of ALDH1 and FOSL1 in glioma patients. Conclusions These combined results demonstrated that TRPM7 induced FOSL1 transcriptional activation, which is mediated by the action of STAT3, a mechanism shown to be important in glioma stemness. These results indicated that FOSL1, similar to GSC markers ALDH1 and TRPM7, is a diagnostic marker and potential drug target for glioma patients.

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Section: Discussionmentioning

confidence: 99%

TRPM7 transactivates the FOSL1 gene through STAT3 and enhances glioma stemness

Guo,

Ramar,

Guo

et al. 2023

Cell. Mol. Life Sci.

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“…Hence, there is potential for miR-455-3p and miR-434-3p to serve as a biomarker for both CHF and sarcopenia. Wang and others investigated the connection between glioma and muscle aging with the goal of glioma prognosis using co-expressed genes ( Wang et al, 2022 ). They discovered seven survival-related genes, including FOSL1, KRAS, STAT3, ALCAM, ERBB2, IFNB1, and EN2, as well as eight co-downregulated miRNAs, three co-upregulated miRNAs, and three co-regulated miRNAs.…”

Section: Regulatory Mechanisms Of Non-coding Rnas In Muscle Agingmentioning

confidence: 99%

The role of non-coding RNAs in muscle aging: regulatory mechanisms and therapeutic potential

Shin,

Kwon,

Suh

et al. 2024

Front. Mol. Biosci.

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Muscle aging is a complex physiological process that leads to the progressive decline in muscle mass and function, contributing to debilitating conditions in the elderly such as sarcopenia. In recent years, non-coding RNAs (ncRNAs) have been increasingly recognized as major regulators of muscle aging and related cellular processes. Here, we comprehensively review the emerging role of ncRNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), in the regulation of muscle aging. We also discuss how targeting these ncRNAs can be explored for the development of novel interventions to combat age-related muscle decline. The insights provided in this review offer a promising avenue for future research and therapeutic strategies aimed at improving muscle health during aging.

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“…Even when EGFR and MET were inhibited, the suppression of FOSL1 phosphorylation was temporary, rebounding within 48 h. Consequently, the rebound led to increased transcription levels of five FOSL1 target genes, namely SPRY2, MMP2, JUN, PLAUR, MMP1, and IL-6, contributing to resistance against kinase inhibitors [48][49][50][51][52][53][54]. FOSL1 serves as a clinical prognostic marker for glioma [21,26,55].…”

Section: The General Roles Of Fosl1 In Glioma and Other Tumor Typesmentioning

confidence: 99%

FOSL1’s Oncogene Roles in Glioma/Glioma Stem Cells and Tumorigenesis: A Comprehensive Review

Khedri,

Guo,

Ramar

et al. 2024

IJMS

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This review specifically examines the important function of the oncoprotein FOSL1 in the dimeric AP-1 transcription factor, which consists of FOS-related components. FOSL1 is identified as a crucial controller of invasion and metastatic dissemination, making it a potential target for therapeutic treatment in cancer patients. The review offers a thorough examination of the regulatory systems that govern the influence exerted on FOSL1. These include a range of changes that occur throughout the process of transcription and after the translation of proteins. We have discovered that several non-coding RNAs, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play a significant role in regulating FOSL1 expression by directly interacting with its mRNA transcripts. Moreover, an investigation into the functional aspects of FOSL1 reveals its involvement in apoptosis, proliferation, and migration. This work involves a comprehensive analysis of the complex signaling pathways that support these diverse activities. Furthermore, particular importance is given to the function of FOSL1 in coordinating the activation of several cytokines, such as TGF-beta, and the commencement of IL-6 and VEGF production in tumor-associated macrophages (TAMs) that migrate into the tumor microenvironment. There is a specific emphasis on evaluating the predictive consequences linked to FOSL1. Insights are now emerging on the developing roles of FOSL1 in relation to the processes that drive resistance and reliance on specific treatment methods. Targeting FOSL1 has a strong inhibitory effect on the formation and spread of specific types of cancers. Despite extensive endeavors, no drugs targeting AP-1 or FOSL1 for cancer treatment have been approved for clinical use. Hence, it is imperative to implement innovative approaches and conduct additional verifications.

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MiR-33a targets FOSL1 and EN2 as a clinical prognostic marker for sarcopenia by glioma

Cited by 4 publications

References 75 publications

TRPM7 transactivates the FOSL1 gene through STAT3 and enhances glioma stemness

TRPM7 transactivates the FOSL1 gene through STAT3 and enhances glioma stemness

The role of non-coding RNAs in muscle aging: regulatory mechanisms and therapeutic potential

FOSL1’s Oncogene Roles in Glioma/Glioma Stem Cells and Tumorigenesis: A Comprehensive Review

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