Open Access

ARTICLE

Interferon-gamma regulates the progression of neuroblastoma cells through interferon-regulatory factor-1

by JING WANG^1,#, JUNFENG XU^2,#, YINGRAN YANG¹, YOUZHENG QIU¹, SHANSHAN ZHANG³, NING WANG^1,3,*

1 School of Clinical Medicine, Dali University, Dali, 671000, China
2 Department of Radiology, The First Affiliated Hospital of Dali University, Dali University, Dali, 671000, China
3 Department of Pediatric Surgery, The First Affiliated Hospital of Dali University, Dali University, Dali, 671000, China

* Corresponding Author: NING WANG. Email:
# Co-first authors

BIOCELL 2024, 48(9), 1343-1353. https://doi.org/10.32604/biocell.2024.051673

Received 12 March 2024; Accepted 11 June 2024; Issue published 04 September 2024

Abstract

Objective: This study aimed to elucidate the influence of IFN-gamma (IFN-γ) in neuroblastoma (NB) cells and reveal its potential underlying molecular mechanism. Methods: The Cell Counting Kit-8, Transwell apparatus, and flow cytometry were employed to assess cellular viability, migratory capacity, invasive potential, and apoptotic rates, respectively. RNA-seq combined with bioinformatics analysis revealed differentially expressed genes (DEGs) and their possible biological functions. Protein levels were determined by western blot analysis. Results: IFN-γ treatment resulted in diminished cell viability, mitigated migratory and invasive capabilities, and augmented apoptotic activity in the SK-N-BE (2) cell line, whereas it exhibited the opposite effect in SH-SY5Y cells. Furthermore, interferon regulatory factor 1 (IRF-1) was the common DEG in both IFN-γ-treated SK-N-BE (2) and SH-SY5Y cells. Additionally, we found that it was underexpressed in NB tissues. The depletion of IRF-1 promoted the progression of both SK-N-BE (2) and SH-SY5Y cells. Moreover, IRF-1 knockdown effectively counteracted the effects of IFN-γ on SK-N-BE (2) cells, while exacerbating them in SH-SY5Y cells. Conclusion: This study verified that IFN-γ exerted a distinct role in both N-Myc-and non-N-Myc-amplified NB cells, partially by mediating the expression of IRF-1, suggesting that it may serve as a potent agent for treating patients with NB.

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Keywords

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