FLCN - A Promising Novel Prognostic Biomarker for Lung Adenocarcinoma (LUAD) Patients

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Abstract

Rationale: The tumor suppressor FLCN gene mutations are the primary cause of the rare autosomal recessive genetic disorder known as Birt-Hogg-Dubé (BHD) syndrome. Early diagnosis of BHD is difficult since FLCN mutation-caused tumors can form in the skin, lungs, kidney, and other organs and are benign. These tumors generate a range of phenotypes. Methods: The UALCAN database was utilized to ascertain FLCN expression and methylation in LUAD. Additionally, using KM plotter, GEPIA2.0, and cBioPortal, respectively, the survival, validity, and mutation analysis of FLCN was ascertained in LUAD. Using STRING and DAVID tools, the pathway and gene enrichment were identified in the presence of FLCN. The muTarget database was used to identify the mutant genes. Results: The goal of the current study is to examine FLCN expression in LUAD tissues. In these patients with LUAD, the study compared the expression of FLCN to other clinic-pathological characteristics. When comparing LUAD patients’ clinical parameters to those of normal control samples, FLCN expression was higher. Additionally, it was discovered that a higher expression of FLCN in LUAD patients was linked to a shorter overall and disease-free survival. Results of gene ontology and pathway analysis demonstrated that genes linked with FLCN are significantly co-expressed with FLCN and are involved in a wide range of distinct molecular functions, biological processes, and pathways. FLCN expression was also correlated with promoter methylation levels, genetic alterations, other mutant genes. This crucial information demonstrated the important function that FLCN plays in the initiation and expansion of LUAD. Conclusion: This research emphasizes how crucial genetic analysis is to the diagnosis and the therapeutic treatment of LUAD.

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