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Original Research Article | OPEN ACCESS

HMGB1-mediated-TLR4/MyD88 signaling regulates cell proliferation, migration and invasion in esophageal squamous cell carcinoma

Xuyang Liang1,2, Yanqin Ma2, Zhimei Zhang2,3, Dazhou Xu2, Shengxiang Lv2, Yanling He4, Shuxian Zhang2, Ling Ren2, Ping Xu1

1Department of Gastroenterology, Shanghai Songjiang Clinical Medical College of Nanjing Medical University, Shanghai 201600, China; 2Department of Gastroenterology, Lianyungang Clinical Medical College of Nanjing Medical University; Lianyungang, Jiangsu 222061, China; 3Phase I Clinical Research Center, Lianyungang, Jiangsu 222061, China; 4Department of Pathology, The First People's Hospital of Lianyungang, Lianyungang, Jiangsu 222061, China.

For correspondence:-  Ping Xu   Email: sjzxxp@yeah.net

Accepted: 27 March 2023        Published: 29 April 2023

Citation: Liang X, Ma Y, Zhang Z, Xu D, Lv S, He Y, et al. HMGB1-mediated-TLR4/MyD88 signaling regulates cell proliferation, migration and invasion in esophageal squamous cell carcinoma. Trop J Pharm Res 2023; 22(4):723-729 doi: 10.4314/tjpr.v22i4.3

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To study the effect of high mobility group box protein 1 (HMGB1)-mediated toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) on esophageal squamous cell carcinoma (ESCC).
Methods: Cell viability was determined using CCK-8 test and colony formation assay, while cell migration and invasion were assessed by Transwell assay. Western blotting was used to determine protein and mRNA expression levels. The effect of TLR4/MyD88 signaling pathway on proliferation of ESCC cells was investigated via in vitro knockdown of HMGB1.
Results: Data from in vitro experiments indicated that HMGB1 knockdown significantly decreased the proliferation, migration, and invasion of EC9706 cells in siHMGB1 group, when compared with siNC group (number of invasive cells in siHMGB1 vs. corresponding number in siNC: 26.7 ± 4.5 vs. 68.7 ± 2.5; p < 0.01), and also decreased proliferation, migration and invasion of TE-9 cells in siHMB1, relative to siNC group (number of invasive cells in siHMGB1 vs. corresponding number in siNC: 29.3 ± 3.5 vs. 55.7 ± 3.1; p < 0.01). Moreover, MGB1 knockdown via siTLR4 transfection significantly down-regulated the expressions of TLR4/MyD88 and epithelial-mesenchymal transition (EMT), but over-expression of TLR4 reversed the inhibition by HMGB1 knockdown on ESCC cells (p < 0.01).
Conclusion: These findings suggest that HMGB1-mediated TLR4/MyD88 signal pathway is a potential treatment route for ESCC.

Keywords: HMGB1-mediated TLR4/MyD88 signaling, Esophageal squamous cell carcinoma, Cell migration and invasion

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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