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Article 24 |\n| --- | --- |\n| 2024\u003Cbr>Investigating the biomarker potential and molecular targets of TIGD1 in lung cancer using bioinformatics\u003Cbr>MERVE GULSEN BAL ALBAYRAK\u003Cbr>TUĞCAN KORAK\u003Cbr>MURAT KASAP\u003Cbr>GURLER AKPINAR\u003Cbr>Follow this and additional works at: [https://journals.tubitak.gov.tr/medical](https://journals.tubitak.gov.tr/medical)\u003Cbr> Part of the Medical Sciences Commons |  |\n\nRecommended Citation  \nBAL ALBAYRAK, MERVE GULSEN; KORAK, TUĞCAN; KASAP, MURAT; and AKPINAR, GURLER (2024)\"Investigating the biomarker potential and molecular targets of TIGD1 in lung cancer using bioinformatics,\" Turkish Journal of Medical Sciences: Vol. 54: No. 6, Article 24. [https://doi.org/10.55730/](https://doi.org/10.55730/)[ ](https://doi.org/10.55730/)1300-0144.5920  \nAvailable at: [https://journals.tubitak.gov.tr/medical/vol54/iss6/24](https://journals.tubitak.gov.tr/medical/vol54/iss6/24)  \nThis work is licensed under a Creative Commons Attribution 4.0 International License.  \nThis Research Article is brought to you for free and open access by TÜBİTAK Academic Journals. It has been accepted for inclusion in Turkish Journal of Medical Sciences by an authorized editor of TÜBİTAK Academic Journals. For more information, please contact [academic.publications@tubitak.gov.tr](academic.publications@tubitak.gov.tr)  \n\n| | Turkish Journal of Medical Sciences [http://journals.tubitak.gov.tr/medical/](http://journals.tubitak.gov.tr/medical/) | Turk J Med Sci (2024) 54: 1369-1380 © TÜBİTAK |\n| --- | --- | --- |\n| | \u003Cbr>Research Article | doi:10.55730/1300-0144.5920 |\n\nInvestigating the biomarker potential and molecular targets ofTIGD1 in lung cancer  \nusing bioinformatics  \nMerve Gülsen BAL ALBAYRAK*􀁋, Tuğcan KORAK􀁋, Murat KASAP􀁋, Gürler AKPINAR􀁋 Department of Medical Biology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkiye  \nReceived: 19.12.2023  Accepted/Published Online: 19.08.2024  Final Version: 05.12.2024  \nBackground/aim: Lung cancer, a predominant contributor to cancer mortality, is characterized by diverse etiological factors, including tobacco smoking and genetic susceptibilities. Despite advancements, particularly in nonsmall-cell lung cancer (NSCLC), therapeutic options for lung squamous cell carcinoma (LUSC) are limited. Transposable elements (TEs) and their regulatory proteins, such as tigger transposable element derived (TIGD) family proteins, have been implicated in cancer development. TIGD1, upregulated in various cancers, including LUSC, lacks a defined function. The aim of our study was to elucidate the biological functions, associated pathways, and interacting proteins ofTIGD1 .  \nMaterials and methods: The GSE229260 microarray dataset was investigated using the GEO2R tool to identify the differentially expressed genes (DEGs) in TIGD1 silenced in A549 lung cancer cells in contrast to controls. Enrichment analyses and protein–protein interaction (PPI) network construction were performed to uncover key pathways using KEGG and STRING analyses. Hub genes were determined through the intersection of DEGs with lung cancer-related genes via Cytoscape software and the cytoHubba plug-in, and their functions were analyzed. Immune and stromal scores of hub genes were also evaluated using the ESTIMATE algorithm.  \nResults: Analyzing microarray data from TIGD1-silenced A549 NSCLC cells, a total of 13 upregulated DEGs and 1 downregulated DEGs were identified. The TIGD1-associated DEGs revealed significant involvement in crucial molecular pathways, including the PI3K/AKT, FOXO, and p53 signaling pathways. The hub genes AKT1, BRAF, SRC, GAPDH, CCND1, CDKN2A, CTNNB1, KRAS, MYC, and TP53 emerged as central regulators of cell proliferation, apoptosis, and protein metabolism. The hub genes exhibited negative correlations with immune and stromal components in the tumor microenvironment, suggesting their potential as biomarkers for lung cancer therapy.  \nConclusion: This study","cbCaiuFsFrPnEZR2","https://ap.wps.com/l/cbCaiuFsFrPnEZR2","pdf",3958051,14,"English","# Background/aim\n# Materials and methods\n## Differential expression and enrichment\n## PPI network and hub gene analysis\n# Results\n# Conclusion\n# Key words","[{\"question\":\"What was the main aim of the study?\",\"answer\":\"To elucidate the biological functions of TIGD1 in lung cancer and determine associated pathways and interacting proteins.\"},{\"question\":\"How were differentially expressed genes identified?\",\"answer\":\"The GSE229260 microarray dataset was analyzed with GEO2R to compare TIGD1-silenced A549 cells versus controls.\"},{\"question\":\"Which molecular pathways and hub genes were highlighted?\",\"answer\":\"The analysis implicated PI3K/AKT, FOXO, and p53 signaling, with hub genes including AKT1, BRAF, SRC, GAPDH, CCND1, CDKN2A, CTNNB1, KRAS, MYC, and TP53.\"}]","Investigating the biomarker potential and molecular targets of TIGD1 in lung cancer using bioinformatics - Article 24 | PDF",1789994542,35]