Clinical Significance of HMGB1 and Autophagy‐Related Genes in Sinonasal Inverted Papilloma

Author:

Zi Jiajia1ORCID,Wei Zhaoxia1,Wang Lin1,Yan Xudong1ORCID,Zhang Shengnan1,Zhao Lijuan1,Li Danyang1,Dong Zihui1,Yu Longgang1ORCID,Jiang Yan1

Affiliation:

1. Department of Otorhinolaryngology Head and Neck Surgery The Affiliated Hospital of Qingdao University Qingdao China

Abstract

ObjectivesSinonasal inverted papilloma (SNIP) is a noncancerous tumor that develops in the mucous membrane of the nasal sinuses. Many malignancies are tightly linked to autophagy, an intracellular self‐degradation mechanism. HMGB1 has demonstrated its ability to modulate autophagy in many pathological conditions. This work investigates how HMGB1 and other genes involved in autophagy contribute to SNIP.Material and MethodsThe study included 45 patients with SNIP and a control group consisting of 28 individuals. In each group, qPCR was employed to examine the mRNA expression levels of genes correlated with autophagy and HMGB1. HMGB1 and genes associated with autophagy were examined for protein expression levels via Western Blot and immunohistochemical staining assays. At the same time, the association between HMGB1 and genes involved in autophagy was discovered through correlation analysis. Furthermore, Krouse staging was utilized for investigating the expression levels of HMGB1 and other autophagy‐related genes at various stages in clinically staged SNIP patients.ResultsLC3B, ATG5, and Beclin1 autophagy‐related genes and HMGB1 were substantially expressed in SNIP. Additionally, there was a positive correlation between HMGB1 and these genes. During various phases of SNIP, the levels of HMGB1 expression and autophagy‐related genes were notably elevated at stage T4 compared with stage T2.ConclusionClinical staging in SNIP is correlated with HMGB1 expression in conjunction with autophagy‐related genes LC3B, ATG5, and Beclin1, suggesting the possibility of novel prognostic indicators.Level of EvidenceNA Laryngoscope, 134:3941–3946, 2024

Funder

National Natural Science Foundation of China

Natural Science Foundation of Shandong Province

Natural Science Foundation of Qingdao Municipality

Publisher

Wiley

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