AI Article Synopsis
Article Abstract
Objective: The aim of the present study was to explore the relationship among Girdin DNA methylation, its high expression, and immune infiltration in human hepatocellular carcinoma (HCC).
Materials And Methods: The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and International Cancer Genome Consortium (ICGC) databases were used to compare Girdin mRNA expression between HCC tissues and normal tissues, and determine the relationship between Girdin expression and HCC prognosis. TCGA database was also used to analyze the expression of Girdin and its methylation status, as well as the relationship between Girdin DNA methylation and HCC prognosis. The Tumor IMmune Estimation Resource (TIMER) database was used to explore the correlation between Girdin expression and HCC immune infiltration.
Results: Girdin expression was elevated in HCC tissues compared with that in normal tissues. The degree of methylation at cg03188526, a CpG site in the Girdin gene body, was positively correlated with Girdin mRNA expression, while high Girdin expression and cg03188526 hypermethylation were both correlated with poor HCC prognosis. Additionally, HCC tissue with high Girdin expression exhibited abundant immune infiltration, and the high Girdin expression was associated with a worse prognosis in macrophage-enriched HCC specimens.
Conclusion: Our findings indicated that Girdin likely functions as an oncogene in HCC and that hypermethylation at cg03188526 in the Girdin gene body may explain the high Girdin expression levels in HCC tissue. Furthermore, we report for the first time that the adverse effects of high Girdin expression in HCC patients may be partially mediated by tumor macrophage infiltration.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7960887 | PMC |
| http://dx.doi.org/10.1042/BSR20204006 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Comprehensive analysis of bioinformatics and system biology reveals the association between Girdin and hepatocellular carcinoma.
PLoS One
December 2024
Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, China.
Introduction: Hepatocellular carcinoma is one of the leading causes of cancer-related mortality worldwide. The actin-binding protein Girdin is overexpressed in various tumors, promoting tumorigenesis and progression. However, the exact mechanisms by which Girdin regulates liver cancer remain poorly understood.
View Article and Find Full Text PDFGIV/Girdin Modulation of Microglial Activation in Ischemic Stroke: Impact of FTO-Mediated m6A Modification.
Mol Neurobiol
November 2024
Key Laboratory of Molecular Biology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou, China.
Ischemic stroke (IS) is one of the most common causes of death in the world. The lack of effective pharmacological treatments for IS was primarily due to a lack of understanding of its pathogenesis. Gα-Interacting vesicle-associated protein (GIV/Girdin) is a multi-modular signal transducer and guanine nucleotide exchange factor that controls important signaling downstream of multiple receptors.
View Article and Find Full Text PDFCXCL12/CXCR4 Axis Promotes the Chemotaxis and Phagocytosis of B Cells through the PI3K-AKT Signaling Pathway in an Early Vertebrate.
J Immunol
December 2024
Guangzhou Key Laboratory of Subtropical Biodiversity and Biomonitoring, Institute of Modern Aquaculture Science and Engineering, School of Life Sciences, South China Normal University, Guangzhou, China.
Chemokines play crucial roles in the regulation of immune cell migration and development. The CXCL12/CXCR4 axis has been extensively studied in mammals, but its regulatory mechanism in teleost fish remains unclear. In this study, we used Nile tilapia (Oreochromis niloticus) as a teleost model to investigate the mediation of the CXCL12/CXCR4 axis in IgM+ B cells.
View Article and Find Full Text PDFmiR-4448/Girdin/Akt/AMPK axis inhibits EZH2-mediated EMT and tumorigenesis in small-cell lung cancer.
Cancer Med
October 2024
Department of Respiratory Medicine, Saitama Medical Center, Saitama Medical University, Kawagoe-shi, Saitama, Japan.
Article Synopsis
- Small-cell lung cancer (SCLC) displays high levels of EZH2, which promotes a process called epithelial-mesenchymal transition (EMT), increasing the cancer's invasive ability.
- Researchers investigated the relationship between microRNAs (specifically miR-4448) and EZH2 in SCLC, discovering that the downregulation of EZH2 leads to increased miR-4448 expression, which appears to inhibit tumor growth and EMT.
- miR-4448 targets the girdin gene to suppress its expression, reducing Akt phosphorylation, which subsequently enhances the phosphorylation of AMPK and EZH2, ultimately preventing EZH2-mediated EMT and tumorigenesis in SCLC.
Growth signaling autonomy in circulating tumor cells aids metastatic seeding.
PNAS Nexus
February 2024
Department of Cellular and Molecular Medicine, School of Medicine, University of California San Diego, La Jolla, CA 92093, USA.
Self-sufficiency (autonomy) in growth signaling, the earliest recognized hallmark of cancer, is fueled by the tumor cell's ability to "secrete-and-sense" growth factors (GFs); this translates into cell survival and proliferation that is self-sustained by autocrine/paracrine secretion. A Golgi-localized circuitry comprised of two GTPase switches has recently been implicated in the orchestration of growth signaling autonomy. Using breast cancer cells that are either endowed or impaired (by gene editing) in their ability to assemble the circuitry for growth signaling autonomy, here we define the transcriptome, proteome, and phenome of such an autonomous state, and unravel its role during cancer progression.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!