# Unveiling the impact of C15orf48 on non-small cell lung cancer through NF-kappa B signaling

## TL;DR

This study shows that the C15orf48 gene promotes non-small cell lung cancer growth and is linked to the NF-kappa B signaling pathway.

## Contribution

The novel finding is that C15orf48 contributes to NSCLC progression via immune cell infiltration and NF-kappa B signaling.

## Key findings

- C15orf48 is upregulated in NSCLC tissues and linked to poor prognosis.
- Knockdown of C15orf48 reduces cancer cell proliferation, invasion, and tumor growth.
- NF-kappa B signaling is a key pathway involved in C15orf48's role in NSCLC.

## Abstract

The role of the C15orf48 gene in lung cancer is not well understood. This study aimed to investigate the effect of C15orf48 in non-small cell lung cancer (NSCLC). Bioinformatics analyses were performed using Oncomine, The Cancer Genome Atlas (TCGA), Protein-Protein Interaction (PPI) networks, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). Immunohistochemical staining was used to detect C15orf48 expression in tissue microarrays. Cellular assays, including CCK8, colony formation, wound healing, transwell migration, flow cytometry, and cell adhesion, were conducted to assess cell viability, proliferation, invasion, and apoptosis. A xenograft tumor model was used to examine tumor growth, and Western blotting was used to detect protein expression. C15orf48 expression was significantly upregulated in tumor tissues compared to normal tissues and was associated with poor prognosis. Knockdown of C15orf48 in A549 and H1299 cells reduced proliferation, invasion, and adhesion while increasing apoptosis. C15orf48 knockdown also inhibited tumor growth in vivo and was associated with immune cell infiltration. Although C15orf48 expression correlated with the epithelial-mesenchymal transition (EMT) score, no significant differences were observed. GSEA identified the NF-κB signaling pathway as a key pathway involved. Proteins PLAUR, IKBα, IL-1RN, ICAM1, and TMPRSS4 showed decreased expression in the shC15orf48 group compared to the shCtrl group. We concluded that C15orf48 promotes NSCLC progression, potentially through immune cell infiltration and the NF-κB signaling pathway.