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      High-Mobility Group Box 1 Overexpression Predicts a Poor Prognosis and Promotes Epithelial-Mesenchymal Transition in Gastric Cancer by Activating TLR4/NF-κB Signaling

      research-article
      a , * , a , b
      Oncology
      S. Karger AG
      Epithelial-mesenchymal transition, Gastric cancer, HMGB1, TLR4, NF-κB

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          Abstract

          Introduction: The molecular mechanism of high-mobility group box 1 (HMGB1) promoting the epithelial-mesenchymal transition (EMT) of gastric cancer (GC) has not been known well. This study aimed to explore the clinical effects of HMGB1 expression levels on the clinicopathological characteristics of patients with GC and to uncover the potential molecular mechanism which promotes tumor progression. Methods: The expression levels of HMGB1 in 125 patients with GC were detected by immunohistochemistry and Western blotting. Univariate and multivariate analyses were performed to evaluate the relationship between HMGB1 expression and clinical characteristics of patients with GC. Stable overexpression (over-HMGB1) and knockdown (sh-HMGB1) GC cell lines (AGS and MKN-45) were used to determine the effects of HMGB1 on the activation of TLR4/NF-κB signaling. Differences were considered statistically significant at p < 0.05 in two sides. Results: HMGB1 is highly expressed in GC tissues and cell lines. High HMGB1 expression (HR = 1.89, 95% CI: 1.44–2.39, p = 0.001) was an independent risk factor for overall survival in patients with GC. Downregulation of HMGB1 resulted in downregulation of TLR4 and NF-κB subunit (p-p65 and p-IκBα) expression, whereas the upregulated expression of HMGB1 led to increased expression of TLR4 and NF-κB subunits. Overexpression of HMGB1 promotes the upregulation of EMT-TF expression, which enhances the proliferation and migration abilities of GC cell lines. Conclusion: HMGB1 is highly expressed in GC tissues and is associated with a poorer prognosis in patients with GC. HMGB1 activates the TLR4/NF-κB signaling pathway to promote EMT progression in GC cell lines. HMGB1 may be a critical molecule in prognosis prediction and a therapeutic target for patients with GC.

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          Author and article information

          Journal
          OCL
          Oncology
          10.1159/issn.0030-2414
          Oncology
          Oncology
          S. Karger AG
          0030-2414
          1423-0232
          2023
          December 2023
          04 September 2023
          : 101
          : 12
          : 786-798
          Affiliations
          [_a] aThe First School of Clinical Medicine, Lanzhou University, Lanzhou, China
          [_b] bDepartment of Surgical Oncology, Gansu Provincial Hospital, Lanzhou, China
          Author notes
          *Mingxu Da, hxdamingxu@hotmail.com
          Author information
          https://orcid.org/0000-0001-9181-6088
          Article
          533927 Oncology 2023;101:786–798
          10.1159/000533927
          37666221
          de9a0316-08ce-4623-83f8-90975042c0a2
          © 2023 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.

          History
          : 26 July 2023
          : 29 August 2023
          Page count
          Figures: 7, Tables: 2, Pages: 13
          Funding
          This study was supported by the National Natural Science Foundation of China (No. 82160588).
          Categories
          Clinical Translational Research

          Medicine
          HMGB1,TLR4,NF-κB,Gastric cancer,Epithelial-mesenchymal transition
          Medicine
          HMGB1, TLR4, NF-κB, Gastric cancer, Epithelial-mesenchymal transition

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