Turkish Journal of Medical Sciences
Author ORCID Identifier
MERVE GULSEN BAL ALBAYRAK: 0000-0003-2444-4258
TUĞCAN KORAK: 0000-0003-4902-4022
MURAT KASAP: 0000-0001-8527-2096
GURLER AKPINAR: 0000-0002-9675-3714
DOI
10.55730/1300-0144.5920
Abstract
Background/aimLung cancer, a predominant contributor to cancer mortality, is characterized by diverse etiological factors, including tobacco smoking and genetic susceptibilities. Despite advancements, particularly in non-small cell carcinoma (NSCC), therapeutic options for squamous cell carcinoma (LUSC) are limited. Transposable elements (TE) and their regulatory proteins, such as Transposable element derived (TIGD) family proteins, have been implicated in cancer development. TIGD1, upregulated in various cancers, including LUSC, lacks a defined function. This study aimed to elucidate the biological functions, associated pathways, and interacting proteins of TIGD1.Materials and methodsThe GSE229260 microarray dataset were investigated using GEO2R tool to identify the differentially expressed genes (DEGs) in TIGD1 was 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 Cytohubba plugin, and their functions were analyzed. Immune and stromal scores of hub genes were also evaluated using ESTIMATE algorithm.ResultsAnalyzing microarray data from TIGD1-silenced A549 NSCC cells, A total of 13 upregulated DEGs and 1 downregulated DEGs were identified. The TIGD1-associated DEGs, revealing significant involvement in crucial molecular pathways, including the PI3K/AKT, FOXO, and p53 signaling pathways. The hub genes, namely AKT1, BRAF, SRC, GAPDH, CCND1, CDKN2A, CTNNB1, KRAS, MYC, and TP53, emerged as central regulators of cell proliferation, apoptosis, and protein metabolism. Hub genes exhibited negative correlations with immune and stromal components in the tumor microenvironment, suggesting their potential as biomarkers for lung cancer therapy.ConclusionThis study elucidates the potential functions of TIGD1 in lung cancer and identifies promising biomarker candidates associated with TIGD1 gene expression, presenting potential therapeutic targets for lung cancer therapies.
Keywords
biomarker, Lung cancer, lusc, nsclc, tigd1
First Page
1369
Last Page
1380
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Recommended Citation
BAL 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/10.55730/1300-0144.5920
Available at:
https://journals.tubitak.gov.tr/medical/vol54/iss6/24